Basic Disc Anatomy:

The intervertebral discs may be thought of as soft and tough pads that

separate the bones (vertebrae) of the spine from one another. Their
basis function is three-fold: 1) they act as a ligament by holding the
vertebrae of the spine together; 2) they act as a shock absorber, which
helps carry the downward weight (axial load) of the body while the
human is in an upright position; and 3)
they act as pivot
point, which allows
the spine to bend,
rotate and twist.
There are 23 discs
in the human spine:
6 in the neck
(cervical region), 12
in the middle back
(thoracic region),
and 5 in the lower
back (lumbar
region). This page
shall focus on the
lumbar spine;
however, the
thoracic and cervical
spines are similar in
make-up.
The disc is made up of three basic structures: the nucleus pulposus,
the annulus fibrosus (aka anulus fibrosus) and the vertebral endplates. Although their composition percentage differs, the latter three
structures are made of three basic components: proteoglycan (protein),
collagen (cartilage), and water. We will learn all about these structures
below.
Figure #1 depicts a Front view (AP) of the lumbar spine. Here we can
see how the discs (blue) lie in between every vertebrae. Spinal nerves
(yellow) have emerged from between every two vertebrae and travel
down the lower limbs to innervate (give life to) the skin and muscle.

Note how the sciatica nerve is formed within the pelvis by branches
from the last three lumbar spinal nerves. It is this giant nerve that
causes so much trouble in many of us chronic pain sufferers. (more
detail here)
Figure #2 Shows a cut-away posterior view of the lumbar spine. Now
we can better visualize how the sciatic nerve is formed and see just how
close the spinal nerve roots come to the intervertebral disc. Any
herniation of the posterior disc may compress the spinal nerve root and
result in severe lower back pain
and lower limb pain (sciatica).
For more information on sciatica
please visit my 'Sciatica Page'.

Axial Disc Anatomy

and Neurology:
The Nucleus Pulposus
(#1) is the water-rich,
gelatinous center of the disc,
which is under very high
pressure when the human is upright--especially in the seated
position. It has two main
functions: to bear or carry the
downward weight of the body
and to act as a 'pivot point' from
which all movement of the lower
trunk occurs. It's third function is
to act as a ligament and bind the vertebrae together. The Anulus Fibrosus
(#2 ) is a much more fibrous structure that that of the nucleus pulposus
("nucleus") and has a much higher collagen content and lower water
content when compared to the nucleus. Its job is to corral or contain the
pressurized nucleus, which would love to squirt out [like toothpaste from
a tube] because of the high pressure that's upon it. It is made of 15 to
25 concentric sheets of collagen, (a cartilage like substance) called the
Lamellae (#9) . The lamellae are arranged in a special configuration
which makes them extremely strong and easily able to contain that
pressurized nucleus pulposus. The Spinal Nerves Roots (aka: Nerve

Roots) (yellow and labeled L5, S1, S2, S3, and S4) and Spinal Nerves
(L4 yellow) are extensions of the brain and spinal cord. Like super
highways the spinal nerves and nerve roots are constantly carrying
electric messages--INCLUDING PAIN SIGNALS--to and from the brain.
The nerve roots exit the spine through bony holes called the
Intervertebral Foramen (aka: IVF) (Red Zone) . As the nerve
roots 'peal-off' from the cauda equina (one sensory nerve root and one
motor nerve root), they head for their respective IVF. (Noteworthy is the
fact that the two delicate nerve root passs very close to the back of the
disc.) Once within the IVF the two nerve roots merge into one Spinal
Nerve. The Spinal nerves are called "mixed nerves" for they contains
both sensory nerve fiber (aka: afferent) and motor nerve fiber (aka:
efferent). After leaving the spine through the IVF, the nerve split into a
posterior division (Dorsal Ramus) and an anterior division (Ventral
Ramus). The Dorsal Ramus connects to the muscle and skin over
the lower back, butt and Facet Joint (#5). The Ventral Ramus
combine in the pelvis and form the giant Sciatic Nerve and Lateral
Femoral Cutaneous Nerve that in turn connect to all the skin and
muscle of the lower limbs. (See my 'Sciatica Page' for more information)
As we will learn below, the ventral ramus has a "recurrent branch" that
connects to the back of the disc, as well as laterally to the sympathetic
nervous system (Grey Ramus Communicans); this special nerve
is called the Sinuvertebral nerve (SN) (see below). In the lumbar
spine (below the L1 disc level) there is no spinal cord. Instead the nerve
roots hang like a horses tail in an enclosed sac, which is called the
Thecal Sac (red stars). The thecal sac, which protects the
dangling nerve roots, is made up of two distinct but tightly bound layers
called the dura mater and arachnoid mater. A clear fluid called
Cerebral Spinal Fluid is also found within the thecal sac. This
fluid protects the nerve roots from pressure injury and also supplies
nutrients. Note how the nerve roots (yellow - S1 - S5), which are
collectively called the Cauda Equina (#4), often have a highly organized
within the thecal sac. Because of this arrangement, which always puts
the lower level nerve root in front, it is possible for a large compressive
posterolateral L4 disc herniation to irritate/compress both the S1 and/or
L5 roots. This may explain why disc herniations do NOT always match
their exact dermatomal distribution; i.e., a disc herniation at L4 may
clinically present as nerve root pain (aka: radicular pain, sciatica) and
dysfunction of both the L4 and/or L5 distributions! The Epidural Space

(#8 ) is the space between the bony neural canal and the thecal sac; or

the space outside of the thecal sac. In reality, this space is filled with
blood vessels and fat and is grossly oversimplifed in figure #9. Note
worthy is the fact that this is the region where 'epidural steroid injections'
are placed. The Facet Joints (#5 ) (aka: zygapophyseal joints) of the spine
are where the vertebrae articulate (join) with each other. Actually, the
gap between the inferior and superior articular processes is the true
facet joint (white region). Collectively the inferior and superior articular
processes and the facet joint are called the Zygapophyseal Joints or
articular pillars. These joints help carry the axial load of the body and
limit the range of motion of the spine. They also make up the back
border of the intervertebral foramen and may physically compress and
trap the exiting nerves secondary to degenerative thickening (sclerosis);
this condition is called lateral canal stenosis. The Ring Apophysis
(#6) is the 'naked bone' of the outer periphery of the vertebral bodies.
The very outer fibers of the disc (Sharpey's Fibers) anchor themselves
into this region. Bone spurs (aka: Osteophytes) may arise from the ring
apophysis as the result of the later stages of Degenerative Disc Disease
(DDD) and/or Osteoarthritis (Spondylosis). Specifically, osteophytes
arise from the prolonged 'pulling and tugging' of 'Sharpey's Fibers' at
their anchor points. The Posterior Longitudinal Ligament
(PLL) (#7) is a strong ligamentous tissue which courses down the
anterior aspect of the vertebral canal and is attached to the outer fibers
of the anulus fibrosus. This highly innervated (supplied with pain
carrying nerve fiber) tissue is the last line-of-defense the posterior
neural tissue has against the irritating and inflammatory effects of
nucleus pulposus.
MRI AXIAL ANATOMY:

Okay, lets see if you have learned anything. Figure #8 is an MRI

over-head view (axial view) of the real anatomy of the L4 disc
and neural structures that you have learned above. Can you
identify the structures?

#1) Disc and

vertebral body of
L4.
#2) Exiting L4 nerve root.
#3) Traversing L5 nerve root. (you can also see the traversing S1
roots as well more posteriorly.)
#4) Thecal sac of the cauda equina.
#5) Facet joint.
#6) Errector Spinalis Muscle.

Remember, this is an MRI T2-Weighted Axial View. You would

not be able to see the nerve root on either the proton density
view or the T1-Weighted view.

SLAB-LAB: NERVE ANATOMY IN AND AROUND THE DISC:

In reality, things don't look so 'nice and neat' within the human body. The
below picture demonstrates what real nerve roots look like:
Figure. #15 is a back view (posterior to anterior) of a real human
cadaver lumbar spine. The back part of the vertebrae (lamina & spinous
processes) have been removed in order to see the dural sac (aka:
thecal sac); the dural sac has been sliced open in order to see the
dangling nerve roots of the cauda equina. Note: the cauda equina is
only seen below the level of L2. Above L2, we have the more familiar
spinal cord.

#1: This ball-like

structure is the ultrasensitive Dorsal
Root Ganglion
(DRG) that contains
the sensory nerve
cell bodies. (the
motor nerve cell
bodies live out of
harms way and are
found in the dorsal
horn of the spinal
cord.) The DRG is
found within the
protective bony
intervertebral
foramen (cut away
in this photo) and
can be
pinched/irritated
from 'far lateral disc
herniations' and/or
lateral canal
stenosis.
#2) This is the
famous 'spinal nerve
root' and is the
number one target
of disc herniation. A
good sized paracentral disc herniation often will compress this adjacent
structure and 'might', if coupled with an inflammatory reaction, ignite the
nerve root into 'anger' and sciatica.
#5) As the spinal nerves leave the spine and head-out into the body to
do their respective jobs, they temporarily join into a mixed spinal nerve
(#5). After this brief marriage, they spilt and become the smaller dorsal
primary rami (#7) (which supplies the skin and muscle of the back) and
the ventral primary rami (#6). The ventral primary rami (aka: anterior
primary rami) of the bottom three nerve roots (L4, L5, and S1), merge
within the pelvis to form the giant 'sciatic nerve', which not only causes

so many of us grief when irritated but, importantly, gives life to the skin
and muscle below the knees.
Inside the dural sac, you can see the free hanging motor nerve root
(#4) and the sensory nerve root (#3). These nerve roots connect into
the real spinal cord about at the L1 level. Pain signals travel along the
sensory nerve root and register 'PAIN' within our brains in the sensory
cortex, among other places.

The Sinuvertebral Nerve: A nerve of mystery

The Sinuvertebral Nerves (SN), is a mixed nerve as well. It
carries both autonomic fiber (sympathetic) and sensory (afferent) fiber.
The sensory portion, which has the capability to carry the feeling of
PAIN, arises from the outer 1/3 of the posterior anulus fibrosus (yellow
balls) and PLL (#7). It then spilts and attaches to both the dorsal ramus
and the grey ramus communicans, although this nerves anatomy and
course seems to be quite anomalous. Of importance is the fact that if
irritated, the nerve ending within the disc have the potential to generate
both back pain and/or lower limb pain (Discogenic Pain). This lower limb
pain-referral has been greatly studied by Ohnmeiss et al. and is quite an
interesting phenomenon. Discogenic Sciatica is the term I have given
this referred discogenic pain. It is believed that the sinuvertebral nerveendings are 'sensitive' to the irritating effects of degenerated nucleus
pulposus, that may be introduced into the outer region of the anulus
from a grade three anular tear. (see may pages on Anular Tears for
more information.) Amazingly, the sinuvertebral nerve also innervates
(connects to) the disc above and below! So, the sinuvertebral nerve of
the L4 disc also innervates the L5 and L3 disc. This may help explain
why a L4 disc herniation/anular tear may clinically present with some
signs of L5 and/or L3 involvement as well. It also carries autonomic
nerve fiber to the blood vessels (not shown) of the epidural space.
Sympathetic nerves control how the blood vessels function (vasomotor
& vasosensory). Although rare, injury to these sympathetic nerves may
cause RSD symptoms in the patients lower limbs; this usually would
occur following surgery. (This may explain why I have a very slight case
of RSD in my left foot following surgery - since my doc spent an hour
cutting his way through a 'nest' of epidural vessels during my microdiscectomy)

The exact pain-pathway (how pain travels from the disc to the spinal
cord) of discogenic pain is another fascinating and controversial subject.
It seems that the sensory pathway from the sinuvertebral nerves into the
spinal cord, does NOT take the 'expected' route in every patient. Some
research (101) has demonstrated that pain-signals travel from the disc,
re-enter the IVF (via sinuvertebral nerve) and DRG at the SAME level.
Other, more recent research has indicated that pain-signals travel from
the disc, through the sinuvertebral nerve, through the Gray Rami
Communicans, into the Sympathetic Trunk (ST), up the
sympathetic chain to the L2 vertebral level (yes I said L2), through the
gray rami communicans, into the L2 dorsal rami, into the L2 IVF, and
into the L2 DRG (80, 81). The latter pain pathway is why some
investigators believe that lower level disc herniations may present as L2
dermatomal pain (groin region) in some patients!
To drive-home my point that the pain path from the disc does NOT
always re-enter at the same vertebral level, I present the 2004
randomized controlled investigation by Oh and shim (26). In an
incredibly well designed outcome study, the latter investigators
demonstrated that by 'cutting' (RF neurotomy) the Gray Ramus
Communicans, the majority of chronic discogenic pain sufferers
achieved substantial relief of their pain and avoid fusion surgery. (26)
This proves that at least some of the incoming pain signals were
traveling toward the sympathetic trunk (which is on the anterior side of
the vertebra) and NOT re-entering the spinal nerves at the same level.

A Committee Error?
Another interesting oddity about the design of the nervous system is the
fact that 'the committee' decided to put the delicate sensory nerve cell
bodies within the IVF and NOT the within spinal cord, which is where the
motor nerve cell bodies are located. The Dorsal Root Ganglion
(DRG), which houses these sensory nerve cell bodies, is seen as a tiny
bulging structure within the IVF. This structure is 'super-sensitive' to
compression (because it houses all these sensory nerve cell bodies)
and can cause extreme back and leg pain if compressed and irritated by
discal material and/or bony outgrowth (stenosis). The placing of these
sensory nerve cell bodies in such close proximity to the disc and within
such a narrow bony tunnel (the IVF) was not 'the committees brightest
idea! You see if you damage the axon (nerve fiber) of a nerve, the
chances are quite good for recovery, but if you damage the 'brain of the

nerve fiber' (nerve cell body) the nerve's chances of recovery are much
less. This explains why patients often never recover completely from
that tingling burning, and numbness following a major attack of sciatica
(disc herniation-induced radicular pain and dysfunction).

The View from the Side: (the Sagittal view)

Fig. #2 Is a sagittal view (aka: lateral view) of the 'motion segment';

Two vertebrae which are 'sandwiching' the

intervertebral disc.
The disc [which is made of a anulus fibrosis
(blue) and the nucleus pulposus (green)] is
made up of three distinct areas: 1) The
nucleus pulposus (green), which is a
water rich (due to proteoglycan aggrecan &
aggrecate molecules which trap and hold
water within the disc) gel in the center of
the disc; 2) The anulus fibrosis (blue),
which is the fibrous outer portions of the
disc that is made up of type I collagen; and
3) The vertebral end-plates (yellow), which are cartilaginous plates
that attach the discs to the vertebrae and supply food (nutrients) to the
inner 2/3 of the anulus and entire nucleus pulposus.
To further increase the strength of the anulus fibrosus, individual sheets
of collagen are layered throughout the anulus. There sheets of collagen
are called lamellae (black curved lines within blue). The very outer
lamellae (Sharpey's fibers), unlike the inner lamellae, are anchored into
the solid bony periphery (Ring Apophysis) of each vertebral body. This is
the region that 'osteophytes' or bone spurs typically like to form. (Click
here to see a real axial view of a 'motion segment'.)

Disc Physiology 101:

The normal human intervertebral disc, which is considered the largest
avascular structure in the human body, is made up of two main
components, proteoglycan and collagen (type I and type II). The anulus
is mostly made of collagen, which is a tough fibrous tissue similar to the
cartilage that is found in the knee, and the nucleus is made mostly of
proteoglycan. Proteoglycans, which are produced by disc cells that

resemble chondrocytes, are extremely important for disc function (see

next paragraph) and are what 'trap' and hold water molecules (H20)
within the tissue of the disc. In fact both the disc and anulus are
comprised mainly of water, i.e., the nucleus is 80% water, and the
anulus is 65% water. Proteoglycans are the building blocks of the
aggrecan molecule which is the true 'water trap' of the disc. Aggrecans
combine within the disc on strands of hyaluronan acid to form huge
structures called 'Aggregates'. These super water-filled proteoglycan
aggregates are what give the healthy young disc its amazing strengths
and pliability, in fact a well hydrated disc is often even stronger than the
bony vertebral body. Fig. #3: Here we have the healthy disc of a
teenager (cadaver). The water content is extremely high as you can
even see by the 'glistening'
appearance of the nucleus
(which is the gray center of
the white disc).

Disc Function:
In order for a disc to function
properly, it MUST have high
water content; this is
especially true of the
nucleus. A well hydrated
(with water) disc is both
strong and pliable. The
nucleus pulposus needs to
be strong and well hydrated to do its job (axial load), for it is this
structure that supports or carries the lion's share of the axial load
(downward weight of body) of the body. With an undamaged anulus,
strongly corralling a fully hydrated nucleus, the disc can easily support
even the heaviest of bodies! As the disc dehydrates (loses water) the
disc loose ability to support the axial load of the body (loses hydrostatic
pressure); this causes a 'weight bearing shift' from the nucleus, outward,
onto the anulus, outer vertebral body, and zygapophyseal joints (facets).
Now, we have an 'over-load' on the anulus (which may trigger other
destructive biochemical reactions) which, if severe and/or is imposed
upon a genetically inferior anulus, will result in pathological DDD. ( see
below)

Hydration also is important with respect to disc nutrition. As we have

already mentioned, nutrients (which all living tissue needs in order to
survive) must diffuse (soak) through the discal tissue in order to reach
the hungry disc cells. This diffusion process is much faster and easier
IF the diffusing tissue has a high water content. We may use
'swimming' as an analogy: It's easier to swim through the water, than
through the sands of a desert. The sands of the desert would be a
dehydrated disc, and the water would be a hydrated disc. So, water
and disc hydration are one of the key factors for a normally functioning
spine and well feed disc.
So, we've learned WHY disc hydration is so important. Now it time to
learn HOW this disc hydration is accomplished:
Water is held within the disc by tiny sponge-like molecules called
proteoglycan aggrecans. These 'super sponges' have an amazing
ability to attract and hold water molecules (324), and can in fact hold
over 500 times their own weight in water; this gives the nondehydrated disc the tremendous 'hydrostatic pressure' which is needed
to bear the axial load of the body. Amazingly, the aggrecans water
absorption is so powerful that over night (non-axial loading) the height of
the disc and the body will actually measurably increase due to the discs
engorgement with water. This phenomenon is called 'Diurnal Change'
and is only present in non-degenerated discs.
Disc cells, particularly the chondrocyte-like cells of the nucleus and
inner anulus, manufacture proteoglycan aggrecan molecules. Like little
factories, they create, replace and rebuild aggrecan molecules. As long
as the disc cells have food (glucose), building material (amino acids)
and oxygen all is well in disc-land. It is also important for them of have
a non-acidic working environment, which is taken care of, since wastes
are diffused out of the disc the same way nutrients diffuse in. In the
living disc up to 100 aggrecans combine on a long piece of 'hyaluronan
acid' to form giant proteoglycan aggregate molecules. It's these
aggregates that are found within the disc in the real world.

Disc Nutrition:
The intervertebral disc is the largest avascular structure in the human
body. The reason for this is because it has no direct blood supply like
most other body tissue. Nutrients (food) for the disc are found within tiny

capillary beds (black arrows) that are in the subchondral bone, just
above the vertebral end-plates . This subchondral vascular network
'feeds' the disc cells of the all important nucleus and inner anulus
through the diffusion process. The Figure on the left shows the 'disc
feeding setup' for disc. Note that the outer anulus has its oven blood
supply that is embedded within the very outer anulus. This is a much
more efficient system and nutrients don't have to diffuse very far to find
their hungry disc cells. The 'more direct' blood supply of the outer anulus
is why tears of the outer 1/3 of the anulus will heal/scar shut with the
passage of time, which unfortunately is not true of the rest of the disc.
Research has indicated that disc tears will not heal in the inner zones of
the disc - probably because of the avascular nature of the inner two
thirds of the disc. Note the nutrients (pink balls) diffuse directly into the
tissue of the outer anulus, where as the nucleus and inner anulus has a
much longer diffusion route that is block by the vertebral end-plates.
Note how the nutrients (pink balls) are released from the blood vessels
(red) in the subchondral bone just under the vertebral end-plates. These
nutrients must 'diffuse' or soak their way through the vertebral endplates and into the disc. This 'diffusion method' is how the cells of the
disc get the nutrients oxygen, glucose, and amino acids which are
required for normal disc function and repair. This poor blood/nutrient
supply to the disc is one of the main reasons that the disc ages and
degenerates so early in life. (Read my Disc Degeneration page for more
information.)
The 'diffusion feeding process' is enhanced somewhat by a phenomena
called 'Diurnal Change'. Our discs have the ability to expand and
compress over the course of a day. As we start the day our discs, like
squeezing out a sponge, will compress and dehydrate because of the
gravity and physical activity which place axial loads upon the discs. In
fact a healthy disc will shrink down some 20% (104), which in turn
decreases our height by 15 to 25mm (194,441,815). As we sleep and
decompress our spines, our discs swell with water plus nutrients and
expand back to their fully hydrated state. This tide-like movement of
fluids in and out of the disc will help with the movement of nutrients into
the avascular center of the disc. (Click here to learn more on Diurnal
Change).
Super Advanced Anatomy & Physiology:

The Nucleus Pulposus:

The nucleus pulposus is a

hydrated gelatinous
structure located in the
center of each
intervertebral disc that has
the consistency of
toothpaste. Its main makeup is water (80%). Its
solid/dry component
make-up are proteoglycan
(65%), type II collagen
fiber (17%) and a small
amount of elastin
fibers . Collectively the
proteoglycans and the
collagen are called the
'nuclear matrix'. The cells
of the disc, which produce
the water holding
proteoglycan molecules
are very similar to
chondrocytes seen in articular cartilage and are also held within the
matrix.
Proteoglycans are found in several structural forms within the disc but
the most important 'arrangement' is called a proteoglycan aggrecan.
These aggrecans main function is to trap and hold water, which is what
gives the nucleus its strength and resiliency. Like a 'super sponge',
aggrecans can trap and hold over 500 times their weight in water!
The nucleus has two functions. The first is to bear most of the
tremendous axial load coming from the weight of the body above and
second to 'stand-up' the lamellae of the anulus - so that the anulus can
reach its full weight baring potential. In order for proper weight bearing
the nucleus and the anulus MUST work hand in hand.
The Anulus Fibrosis:
The anulus is the outer portion of the disc that surrounds the nucleus. It
is made up of 15 to 25 collagen sheets which are called the 'lamellae'.
The lamellae are 'glued' together with a proteoglycans. These sheets

encircle the disc and, in concert with the

nucleus, give the disc tremendous axial
load strength.
The posterior portion of the anulus if
further strengthened by the 'posterior
longitudinal ligament'. This structure is
the final barrier between the disc and the
delicate spinal cord, and nerve roots.
The biochemical make up is similar to that of the disc only in different
proportions. The anulus is 65% water, with the collagen, both type I and
II making up 55% of the dry weight, and proteoglycans (mostly the
larger aggregate type - 60%) making up 20% of the dry weight. 10% of
the anulus also contain 'elastic fiber' that are seen near where the
anulus attaches into the vertebral end-plate.
The lamellae are made up of both Type I (very strong type) and Type II
collagen fiber. The very outer lamellae are almost all Type I. As we
move inward toward the nucleus the more Type II is seen and less Type
I. The very inner layers are very hard to distinguish from the
nucleus. There is not a clear boundary between the nucleus and the
anulus.
A simply amazing fact about the lamellae design is that the collagen
fibers that make-up each lamellae all run parallel at a 65 degree angle
to the sagittal plane. Even more amazing is the fact that the each
lamellae are flipped so that the 65 degree angle alternates between
every lamellae, one to the right then one to the left. This design greatly
increases the shear strength of the anulus and makes it had for cracks
to develop through the layers of the anulus. This is just amazing if you
think about it!! Brilliant design!
The function of the anulus is to help the nucleus support the axial weight
from the body. The anulus does need some help from the nucleus in
order to achieve its strongest configuration. It relies on the nucleus to
push it outward which keeps the lamellae from collapsing inward. The
nucleus must keep a very high hydrostatic pressure to achieve this. We
saw what happens when the nucleus losses hydrostatic pressure under
the 'Disc Degeneration' page. Bogduk used the analogy of a rolled up
telephone book standing on end, to describe how strong the anulus
could be when the nucleus holds the inner lamellae or phonebook in a

rolled up position. If you unroll the phone book our 'on end phone book'
it would not longer be able to support much axial loading.
The Vertebral End-Plates:
Both the top and the bottom of each vertebrae (spinal bones) are
capped with a thin millimeter cartilaginous pad called the 'Vertebral
End-Plate' (Figure #1). Despite their name, these end-plates are NOT
attached to the subchondral bone of the vertebrae but are instead
strongly interwoven into the anulus of the disc (156, 388). It is for this
reason, as well as strong morphological similarities, that the vertebral
end-plates are considered part of
the disc and NOT part of the
vertebral body.
The biochemical morphology of the
end-plates is extremely similar to
that of the disc: Water,
proteoglycans, collagen and
cartilage cells (chondrocytes). The
concentration scheme of these
components also mirrors that of the
disc: The center of the end-plate is
mostly water and proteoglycan. As
we move outward toward the
periphery, more and morecollagen
is seen with less and less
proteoglycans. This similar
biochemical makeup and distribution scheme helps the diffusion of
nutrients between the subchondral bone of the vertebra and the depths
of the disc.
The very outer rim of the vertebrae is NOT covered by the end-plate,
which leaves a ring of exposed bone on the periphery of the top and
bottom of each vertebra. This exposed peripheral area is called the
'Ring Apophysis' and is often a site for the development of spur
formation associated with the degeneration process.

Basic Anatomy:
I've already covered the axial disc anatomy at nauseam on my
'Disc Anatomy
Page'. Please go
there first if you are
not comfortable
with the structures
of the disc.
The key structures
of the axial (overhead) MRI are as
follows: The
Thecal Sac, the
Exiting Spinal
Nerve Roots
(L5), and the
Traversing
Spinal Nerve
Roots (S1 ). All of the preceding structures all have the capability
to generate PAIN within the patient, if they become irritation (from
biochemical which leak from the disc - cytokines) and/or
compressed.
The axial view is the only true way to visualize just what structures
are being compressed and by what, although the sagittal view can
'grossly' demonstrate compression and herniation/bulging.
Unfortunately, as you will learn below, MRI images are not as well
demarcated as my drawing to the right of us! Sometimes you have
to "hallucinate" a little. (All you MDs and DCs will know just what
I'm talking about!)

Who's On First? How To Tell What Disc is What:

The Scout Image

Without the "scout image", it will be near impossible for the

layperson to distinguish the difference between any of the 5 discs
of the lumbar spine. The scout image is like a road map that tell
you which slice is what and is almost mandatory for even the most
experience doctor to have.
Here we have a "scout image" that identifies 20 'cuts' or slices
through the sagittal lumbar spine. Each number is assigned to the
MRI image that
was taken along
that plane. These
images only cover
discs L3, L4, and
L5 in this example.
For example, slice
#11 (one line
above 10 which is
colored red to help
you) goes right
through the L4 disc
and is the image to
look for if you have
a L4 disc problem.
Image 18 (line 18) would correspond with the L3 disc and Image 5
is the best cut through the L5 disc.
On a patient with a greatly thinned disc, It would be better to ask
for 'thinner slices' (6mm should do) in order to insure that you get a
cut through the thinner disc. In this case, my L5 disc
So, if you want to e-mail me an image of your disc, now you know
how to find the image by using the scout image. On some MRI
films, a tiny scout image is built right in to each bigger image. This
makes it very easy to tell what disc you are looking at.

MRI Anatomy: The Axial Views.

Figures #10 & #11 are over-head views (aka: axial views) of the
L5 disc. Although this patient does have a moderate degree of disc
degeneration (black disc) and a small non-compressive 4
millimeter central disc herniation, he had a very large 'central canal'
which nicely demonstrates the axial MRI anatomy.
The nucleus pulposus is not visible on these images. One reason
for this is because the disc has too much desiccation to distinguish
between the anulus and nucleus, and the other reason is that this
is a T1 Weighted image (higher resolution) with will not differentiate
between the high water content of the nucleus and the more arid
anulus; however, on a normal, non-degenerated disc, you can

easily see a nuclear region and a anular region on the T2 Weighted

image (see Figure #7).
The 'posterior neural structures' include the Traversing Nerve
Roots, the Thecal Sac (dura and arachnoid mater) and the
Exiting Nerve Roots that lie within the IVF (pink zone) and

not very visible on this particular image. If you 'hallucinate' a bit,

you can see a 'Mickey Mouse' like orientation, where the thecal sac
is the head and the traversing spinal nerve roots are the ears.
Again, note that despite the 4mm disc protrusion, there is no
contact between the traversing S1 roots and the herniation in this
patient. (I wish I had this much room in my central canal!) Often
times a disc herniation or scar tissue will 'blot-out' one of the
traversing roots (Mickey's Ear); this is often a sign of nerve root
compression.
Figure #7 demonstrates
another axial view of a
normal health L4 disc from
a 45 year-old-male.
Now we can see a distinct
nuclear region and a
surrounding anular region.
Note that 'Mickey Mouse' is
no longer visible at this
level. Also note the
concavity of the posterior
disc adjacent to the
traversing L5 nerve roots.
This is the sign of a healthy
disc. The exiting L4 nerve
roots can be seen farther
laterally. It is very important
to understand that in the
lumbar spine, BOTH the
exiting nerve roots (L4 roots
at this level) AND the
traversing nerve roots (L5 roots at this level) may become
compressed via large disc herniation and/or severe stenosis.
In this particular image, you can clearly see the tiny nerve roots
hanging in a semi-organized fashion within the thecal sac (L5 roots
and S1 roots).

Note the neuroforamina are wide open (light yellow zone) and
demonstrate no evidence of major stenosis from the adjacent facet
joints.
T2 Weighted images are always best for visualizing Degenerative
Disc Disease. This is because the T2 image shows off watery
structures as bright white and shows off desiccated regions (areas
with low fluid concentrations) as black.

Okay, lets move on to some other stuff. Remember, if you need a

over-view of the anatomy, please visit my 'Disc Anatomy Page'.

The Sagittal Image Anatomy: View from the

Side.
Figure #8 is a view of the lumbar spine from the side, or a
Sagittal Image. Note that this particular image is, contrast
wise, in between the T2 image and T1 image; it's called a Proton
Density Image and is the absolute best image to denote
whether or not a disc herniation has 'extruded' through the
posterior longitudinal ligament (PLL). It, like the T1 image, is done
at high magnification,hence it's detail is amazing.

First the basic structures: The

discs, which are stationed
between the vertebrae, should
be a white color (hydration).
Note the 'blackness'
(desiccation) of the L5 disc
(disc between L5 and sacrum);
this represents moderate to
severe degenerative disc
disease. The PLL (tiny blue
arrows) appears as a black
vertically orientated line
running down the posterior
surface of the vertebral bodies
and disc. Note that, amazingly,
despite this patients 9mm disc
herniation (white HNP), the
PLL is still 'containing' the
protruding nuclear material and
has not appeared to have
ruptured, although it is certain
uplifted from the bone, as
nuclear material is seen above
level of the disc space. This would technically be called a large
contained disc extrusion.
The thecal sac (red stars) is the 'super white' structure that fills the
central spinal canal just behind the posterior vertebral bodies. This
sac house the free-floating spinal nerve roots (cauda equina) and
is made up of both motor and sensory nerve fiber.
The ligamentum Flavum (green star) courses between each of the
vertebrae and adds stability to the spine. This structure can
hypertrophy or thicken in some patients and help to cause the
dreaded central canal stenosis, which is the nemesis of the
elderly.

Zones of the Anterior Epidural Space:

Herniation Zones.
Now, let's use some CT axial images (my own) to learn the
different regions of the anterior epidural space; the regions where
disc herniation occur in. If you have ever read your MRI report,
some of these terms may sound familiar, for these are regions
(zones) are often used by radiologists to describe the exact
location of your disc herniation.
BLUE: This is the 'Central Region' and is located directly
behind the disc and encompasses the anterior aspect of the thecal
sac. Since the PLL (posterior longitudinal ligament) is at its thickest
in this region, the disc usually herniates slightly to the left or right of
this central zone. (As a side note, I would add that if you do have a
centrally located disc
herniation, the
chances of a
successful
discectomy are
reduced.)
PINK: This is the
'Paracentral
Region' or
'Lateral Recess'
and is located just
outside of the Central
Region. Because the
PLL is not as thick in
this region, disc
herniations are
frequently found here;
in fact, this is the
number one region for
disc herniations to
occur in. The Traversing Nerve Roots, which are the neural

structures found in this zone, are frequently contacted, deviated

and compressed in this zone. (Remember, an L5 disc herniation
that occur into the lateral recess with compress the traversing S1
nerve root, not the exiting L5 nerve root that lives within the IVF.)
GREEN: This is the 'Intraforaminal Zone', also known as the
'Subarticular Zone', and is located within the intervertebral
foramen (IVF). It is fairly rare for a disc to herniate into this region
or beyond; in fact, only 5% to 10% of all disc herniation occur here
or farther out. (241-244) When herniations do occur in this zone,
they are often very troublesome for the patient. This is because a
super-delicate neural structure called the 'Dorsal Root Ganglion'
(DRG) lives in this zone. Any compression of the DRG can result in
severe pain, sciatica (aka: radiculopathy) and nerve cell body
(neuron) damage.
YELLOW: This is the 'extraforaminal zone' and, as the name
implies, is just outside (lateral to) of the IVF. Again, it is very rare for
a disc to herniate into this region, but when it does happen, it is
often very troublesome for the patient and surgeon. A herniation in
this zone may also irritate the 'Sympathetic Nervous System' and
cause RSD like symptoms in the lower limb.

Axial CT Myelogram: Anatomy and

Herniation.
Let us now look at some CT Myelogram images (mine). The first
image (left) is from a 'slice' (remember, CT and MRI images are all
thin cuts through the spine in different planes) just above the L5
disc, through the inferior region of the vertebral body. Since the
'slice' is above the level of the disc, you will only see the posterior
neural structures and not the disc itself.

Note the bright white

'ring apophysis' (not
labeled) that out-lines
the vertebral body more so anteriorly (top
of the picture).
Note that the cauda
equina (thecal sac) is
completely filled with
'white' contrast
material (injected
during my myelogram)
that makes the thecal
sac (dura and arachnoid
mater that surrounds
the cauda equina) and
the 'Dural Sleeves'
(which contain the
spinal nerve roots)
bright white. Since the contrast only fills the root sleeves up to the
DRG, the DRG of L5 is not well visualized. I've placed a black line
in the center of each DRG (dorsal root ganglion).
Also note the facet joints (oblique black slits - labeled) which are
sandwiched between the superior articular process of the sacrum
and the inferior articular process of L5.

The next CT slice (right) is a little be lower than the slice above and
demonstrates the posterior of the disc quite nicely. Now you can
plainly see the posterior disc has both bulged and herniated into
the left traversing S1 nerve root, hence blotting it out (not white in
color like the right S1 is).

I've high-lighted
the posterior ring
apophysis (white
thick 'smile' line) to
demonstrated how
a diseased disc
can 'bulge'
outward. Anytime
disc tissue is seen
outside of the
posterior vertebral
body (ring
apophysis), the
disc is considered
to be 'bulging'.
Bulging discs are
usually no greater
than 2 or 3
millimeters (mm)
and are
'concentric' or
'non-focal' in shape.
My disc bulge has an out pouching or eccentric component to its
shape, as noted by the portion that has moved into the left 'Lateral
Recess'. This out-pouching's is the herniation component to my
disc lesion, and it has made my left S1 root disappear because its
failed to properly fill with contrast - probably due to compression of
that root at this level. (Note the white Nike swoosh just under the
"S1" on the left, affected root. This is contrast material that
"accidentally" leaked into the epidural space following my
myelogram. This wasn't suppose to happen be created a semiepidurogram effect.)
Here is that same image - the L5 disc level - without all the
markings. Try and practice looking at the disc yourself without the
aid of my boundary markers. Can you see the herniation? I bet
you can now! This is considered a broad based herniation for its
base it bigger than its anterior to posterior projection.

One thing to keep

in mind: CT
myelogram's are
designed to look
for 'filling-defects',
and are not really
the best imaging
system for
evaluating the
human disc. The
MRI is much better
at visualizing the
disc.
On a CT
myelogram (left), if
the disc herniation
is large enough it will make the nerve roots turn black, or disappear
(like it does to my left S1 root - only its confusing for you still see
that tilted 'C' of white - which is only the outline of the black,
contract-free, left S1 root). This is because the compression upon
the nerve root will NOT allow the contract material to 'fill' into the
nerve, hence, no bright white nerve root. That spells TROUBLE!

9MM DISC HERNIATION: A Real Case.

Figure #6. demonstrates a large 9mm disc extrusion (red star) as
visualized on both the T1 Axial (over-head) and Sagittal (side)
views.

Note that this extrusion has completely blotted out (can't see) the
right traversing S1 nerve roots (left side of image) and has pinched
it against the lamina (tiny green arrow). Note the thecal sac is
moderately to severely compressed by this large herniation, as
noted on both the axial and sagittal images (between blue arrow
and red star).
This young man (24 years) has avoid surgery and is doing fairly
well, although his days of heavy work are probably over for
good.Note the central canal of this young man is much smaller that
that of the young man in figure 10 and 11. That just pure genetic
folks; bigger central canals are much more forgiving for disc
herniation, that smaller ones.

Practice test: Let's see what you have

learned!

1) On the below MRI

axial image of the L5
disc, name the
structures that are
numbered.
2) Name me the
location of the 'disc
lesion' using the
correct zone.
3) Which nerve root
is being displaced by
this disc lesion?
4) bonus: What type
of MRI image are we
looking at??
hint: T1, T2, or
Proton density??
5) What two structures are being contacted by this disc lesion?

GOOD LUCK! Make sure you look at the answers via the link
below. I've got the case history to go along with the quiz MRI,
including his lateral view, and the official MRI report.

Get the Quiz Answers 'Here'.

General Information on DDD and Disc

Aging:
Unlike other tissues of the human body, the poorly vascularized intervertebral
disc tends to undergo degeneration of its internal structure at a surprisingly early
age. In fact, award-winning research has demonstrated such degeneration
usually begins within the first decade of life! (6,15) Thankfully, most of the time
this degeneration is harmless and considered just part of the natural aging
process. However, in some folks, the degeneration process runs amuck and
spells the proverbial "beginning of the end" for the disc as it leads to destruction
of the disc and chronic pain.(8,14,151,152) Why some people's discs succumb to
such severe disc failure (above right) and pain and others don't continues to be a
mystery, although heredity certainly plays a significant role in this process. It is
this abnormal accelerated form of pathological disc aging and degeneration that I
called Degenerative Disc Disease (DDD). The figures above

demonstrate the difference between normal (left) and severely

degenerated (right) lumbar discs. Note the moderate to severe loss
of disc height (right); a conditions that is called discopathy or
(when in combination with arthritic change) discogenic
spondylosis. The loss of disc height often causes the secondary
problem of
stenosis: the
closing of the
holes where the
spinal nerves,
nerve roots and
spinal cord
reside.
One physical cause
of DDD, and natural
disc aging for that
matter, is poor
disc nutrition.
As you may remember from the disc anatomy page, the majority of disc tissue
has no blood supply (it's avascular). The disc gets its food (nutrients) via diffusion

from blood within the upper and lower vertebral endplates. Normally, the nutrients
pass from the endplates through tiny pores the into the hungry discs. Arthritis of
the endplate (sclerosis) has the negative effect of decreasing the diameter of
these pores, which in turn decreases the rate of food-flow to the disc, which in
turn causes the disc to die, i.e., DDD. In fact, recent award winning scientific
investigations (700, 5) have confirmed the foregoing explanation of disc
degeneration.
Therefore, any attempts at injecting new disc material into a degenerated disc
(such as live disc cells)--in hope of healing the damaged disc--will only lead to
failure, for the new disc material will soon meet the same fate of the original disc
tissue: it will starve to death.
Research has also demonstrated that DDD is associated with pain-producing
conditions of the spine such as annular tears, disc protrusions and spinal
stenosis (201,206,219,227). In fact, in 10% of the population, DDD will result in
permanent chronic pain and life-long disability (250-253). Technically it's not the
actual process of DDD that results in chronic pain, it's the evil "end-phases" of
the disease that cripples these unfortunate few. These end-phases, as
mentioned above, include annular tears (aka: Internal Disc Disruption or IDD)
(203,209,216,231); disc protrusions (227); nerve in-growth (900,904,905,906);
and stenosis.

The MRI Appearance:

The diagnosis of DDD is best made on T2-weighted MRI imaging (Fig.#1) (27),
although some of the late appearances of DDD (disc collapse, osteophytosis,
and sclerosis) may also be seen on CT scan and X-ray. Such MRI appearances
are easy to spot and are characterized by a loss of signal intensity (loss of
whiteness) of discal tissue, which makes the disc appear black instead of
bright white. Technically, this blackening of the disc(s) occurs because the disc
has dehydrated (lost water content) and is dying. This 'blackening' is called disc
Desiccation. Since the MRI signal intensity (whiteness) is directly related the
disc's water content (215,226), any loss of discal water will proportionally
decrease the 'whiteness' of that disc on T2-weighted MRI. So, in layman's
terms, the dryer the disc, the blacker and more degenerated it will look on MRI.
Figure #1: Here is the classic presentation of DDD as seen in this T2weighted sagittal (lateral) image. Note the bright white and healthy L3 disc
(above the L4 vertebra) in comparison to the 'black' and desiccated L4 and
L5 disc. Also note a 4mm herniation at the L4 disc (between L4 and L5
vertebrae) and a 9mm herniation at the L5 disc. Also note there is a loss of
disc height at both L4 and L5, in comparison to the thicker L3 disc.

Why some discs prematurely

degenerate (DDD) and cause chronic
pain and others don't is still somewhat
controversial, however, it is becoming
clearer that poor genetics (397399,403,413a); a past history of
moderate to severe spinal trauma; or
have an occupation that is heavy, and
labor-intensive are the main risk
factors (201,16). These factors will
be discussed in depth below.
Warning:
In order to really understand DDD and
disc aging, you must understand a
few basic principles of disc physiology.
I'm going to assume that you
understand normal disc physiology
and anatomy. If you don't please go
(here) and learn your basic structures,
and more importantly, learn the basics
physiology of the disc. You will need
to know why water (hydrostatic
pressure) is so very important for
normal disc function (allows the
nucleus to support the axial load of the body), and how the cells of the disc
maintain discal water content (via proteoglycan aggrecan production)
In order to understand DDD, we must first understand the natural disc aging
process, or the 'normal pathway' of degeneration, which occurs in all humans to
varying degrees and does NOT lead to pain.

NATURAL DISC AGING: (aka: NDA)

The most common and striking feature of disc aging and degeneration is the loss
of the proteoglycan molecule from the nucleus of the disc (333, 26). Other
findings of aging include a progressive dehydration (18), a progressive thickening
(via cross-linking, glycation and CML formation), brown pigmentation formation
(66) and increased 'brittleness' of the tissues of the disc (62).

The Two Main Factors of Disc Aging:

There are two main factors that are involved in the aging process of the disc and
both of these factors are amplified because of the already poor vascular supply
of the disc:
1) Idiopathic blood vessel/nutrient loss and dehydration:
The short version: For unknown reasons the nucleus of the disc losses much of
its vital blood supply during the first decade of life (6). Without sufficient
nutrients (which are contained in the blood) the cells of the disc begin to die (500)
and the disc (especially the nucleus) becomes depleted of water. The drop in
water/proteoglycan content is one or the classic signs of disc aging (333).
Because of this dehydration of the nucleus, there is ultimately a 'weight-bearing
shift' that occurs from the nucleus onto the outer annulus, ring apophysis, and the
zygapophyseal joints. This increase stress upon the preceding posterior
structures may lead to further more severe forms of aging, i.e., DDD.
The long version: Under the physiology section of the 'Disc Anatomy' page, we
have learned how important disc nutrition is in maintaining a normally functioning
disc. To recap: as long as the cells of the disc receive an adequate nutrient
supply (which is obtain from the diffusion of oxygen, glucose, and amino acids
[pink balls] from capillary beds just above the end-plates, into the disc), they will
happily manufacture the proteoglycan molecule, which combines within the disc
to form the larger aggrecan and aggregate molecules. It is these aggrecan
molecules that trap and hold water within the disc. A fully hydrated disc will
have a very high hydrostatic pressure (osmotic pressure) which makes the
nucleus pulposus (which is 80% water in a normal disc) incredibly strong and
able support the lion's share of the axial load from the body.
Remember, the nutrients in the inner annulus and nucleus have a 'crummy
feeding system' to being with. As you can see on the model on the left, the
nutrients (pink balls) have a long way to 'diffuse' in order to reach all the disc
cells.

Without an adequate supply of

nutrients, the cells of the disc will
die. The preceding fact was
substantiated by the 2001 Volvo
Award winning study of Horner
and Urban (500), who studied the
viability of living human disc cells
under different conditions. They
concluded that if the cells of the
disc failed to get proper nutrients such as oxygen, or glucose - or if
the pH level of the disc rose
(because waste is not being
diffused out of the disc), disc cells
would die and stop producing the
vital proteoglycan molecule;
without proteoglycans, the disc
losses its water content
(dehydrates) and losses its
hydrostatic pressure (osmotic
pressure) (241). This lost
proteoglycan content is the most
striking feature of disc aging and degeneration (333). Other research has
confirmed this cell death as well. In 1982, Trout and Buckwalter discovered that
by adulthood over 50% of the cells of the disc were dead (321).
So what's killing the disc cells and resulting in this loss of proteoglycan content?
Starvation! It seems that the human disc becomes 'nutritionally compromised'
from the moment we begin to stand and walk. In 2002, Boos et al. observed an
idiopathic "obliteration" of portions of the nutrient-providing capillary beds, which
lie just above the vertebral end-plates. (Remember that these capillary beds are
the ONLY source of nutrients for the cells of the inner annulus and nucleus.)
Amazingly, this 'auto-destruction' begins within the first two years of life, and
worsens over the next 8 years. Specifically, they stated that between the ages
of 3 and 10 there was "a dramatic decrease of physiologic vessels in the endplate..and an abundance of areas with obliterated vessels. and a substantial
increase in (disc) cell death." (6) THESE FINDINGS WERE THE 'SMOKING
GUN' that scientists had been waiting for and suggested that the initial causation
of disc aging and degeneration was 'nutritional compromise', secondary to an
idiopathic loss of the discal blood supply above the vertebral end-plates.
Needless to say, Boos and company won the '2002 Volvo Award in Basic
Science' for this most shocking discovery.
Other factors affecting disc nutrition via diffusion rates of nutrients through the
vertebral end-plates include end-plate calcification (506, 537, 538, 552,), the

effects of changes in blood flow patterns secondary to arterial stenosis (522, 524527), smoking, diabetes, and exposure to vibration (500, 517).
The Vicious Cycle of Disc Aging:
This progressive loss of proteoglycan and dehydration begins to 'snowball' out of
control. Not only because of the progressive loss of nutrients, but also because
of the fact that decreased hydrostatic pressure also slows the production of
proteoglycan by the disc cell (11). Here's what this vicious cycle looks like:
As the nutrient supply within the disc drops (because of blood vessel obliteration
and later end-plate mineralization), the disc cells start to die. Because there are
fewer available disc cells around to make proteoglycan, there is a drop in the
amount of circulating proteoglycan aggrecan molecules. This decrease in the
aggrecan molecule, (which is what holds water within the disc) results in both
dehydration, and a decrease in hydrostatic pressure within the nucleus. The loss
of hydrostatic pressure has two negative effects on the disc: a) it will cause a
further decrease in the amount of circulating proteoglycan aggrecan molecules,
for we know from the work of Handa et al. that disc cells need a constant
hydrostatic pressure level of 3 atm to function normally (11). Any increase or
decrease in hydrostatic pressure caused a reduction proteoglycan production,
which in turn decreases hydrostatic pressure even more - hence the vicious
cycle. b) Now, these biochemical changes begin to change the biomechanics of
the disc: With the decrease of hydrostatic pressure the nucleus, like a deflating
beach-ball, can no longer carry the full axial-load (weight) of the body. A 'shift' in
the axial-load distribution begins to occur, with the periphery of the disc (outer
anulus, ring apophysis, and zygapophyseal joints) taking on more and more of
the load and stress. Experimentally, the anulus of a degenerated disc shows a
very high 'stress-load' on the anulus and NOT the nucleus (17 ,12 ). We will
later learn that this 'load-shift' can be greatly accelerated if the volume of the
nucleus is increased by trauma-induced structural damage to either the end-plate
(compression fracture) and/or tearing of the inner anulus.
2.) Non-Enzymatic Glycation & the aging process: Glycosylation (aka:
Glycation)
Glycation (aka: Glycosylation , or non-enzymatic glycation) is a biochemical
reaction which occurs when reduced sugars (like glucose) come in contact with
proteins (like disc collagen) in an avascular environment. The more avascular
the tissue, the more severe this reaction occurs. Since the disc is the largest
avascular tissue in the body, the glycation process thrives within its substance
and results in a slow but steady transformation of disc collagen into a thicker and
more brittle substance. Specifically, this reaction occurs between the protein
molecules within the collagen, and free floating glucose (reduced sugar). This
reaction is called 'posttranslational protein modification' or simple Glycation.
Here's how it works: In the absents of oxygen, reduced sugars start to 'rub

against' (bind) the proteins within the collagen. The proteins can only take so
much 'rubbing', and soon are transformed into what is called an 'Advanced
Glycation End-Product' or AGE. These converted discal collagen strands
(AGEs) become much more brittle and also much more 'sticky', i.e., they love to
combine with their glycated neighbors in a process called 'cross-linking'. This
'cross-linking'
phenomenon
makes the disc
thicker, more
fibrous and more
susceptible to the
development of
DDD (62). It also
stains the discal
tissue a distinct
shade of brown
(66) as noted in
figure #2.
Fig. #2: Here we have early disc aging. The tissue of the disc has turned
brown, secondary to the glycation process, and the disc has become much
'drier and still that the disc seen in adolescents. For comparison sake,

Fig. #3 shows us what the disc of a teenage looks like. Note the well
demarcated, wet looking,
nucleus (gray center) and NO
ugly brown tissue. Ah to be
young again!
Finally, the unstable AGEs
molecules, which produce
another evil biochemical called
the 'free radical', oxidize into a
much more stable structure
called a CML (NCarboxymethyl -lysine). CML
formation has been found to be
an excellent indication of discal
aging (15). In fact Andreas and
Boos won the 1997 Volvo
Award for their work in using the presents of CML-modified discal protein as an
indicator for the various stages of aging (15). I'm not going to review this study
for it's out of our scope, but for those of you who need-to-know, his paper is an
excellent read.

Well, that about does it for the natural aging process of the disc. Let's now take
a look at the more serious form of aging, DDD.

Internal Disc Disruption (AKA - IDD): A General

Overview
Just because that MRI of yours was deemed "normal" by your
doctor does NOT always mean that your back and leg pains
aren't coming from problems within that very disc. This is
especially true if your supposedly normal MRI demonstrates a
bulging and/or 'Black' appearing disc on T2 Weighted MRI
images (132).

In his 1986 presidential address, Dr. H. V.

Crock told members of the international
spine society that 'internal disruptions'
within the architecture of the disc could
result in back pain and even lower limb
pain without the presence of spinal nerve
root compression (9). He termed this
condition "Internal Disc Disruption," herein
IDD. IDD occurs when the disc develops a
rip or tear (or in medical language, a full
thickness radial annular tear ) that bisects
the disc from inside to outside and allows
communication between the jello-like
center [nucleus pulposus] and the nerveinfested periphery of the disc [annulus
fibrosis].
Fig.#5 demonstrates such an annular tear
within a real human cadaver disc. The
white arrows demonstrate a full thickness
radial anular tear within the L4/5 disc that
completely bisects it. Note also that the
disc above (the L3/4 disc) has a small tear in the outer fibers of the annulus
(black arrow) that has not made it (yet) into the middle of the disc. This type of
tear is called a 'rim lesion'.
To understand how IDD may causes 'pain', you will need to know some basis
disc anatomy. I've covered anatomy ad nauseam 'here', but if you're too lazy to
go there, I'll give you a quick refresher here:
Fig.#4 demonstrates the normal lumbar disc anatomy: Here, in this over-head
view, we have the nucleus pulposus (pink) surrounded by the the stronger anulus
fibrosus (green). Normally, the anulus fibrosus is strong enough to corral the
pressurized nucleus pulposus and keep it from escaping outward. Of particular
interest to upcoming discussion is the tiny 'Sinuvertebral Nerves Endings' (yellow
poke-a-dots) that are embedded within the substance of the outer 1/3 of the
anulus fibrosus. We know through scientific investigation that these nerve fibers
have the ability to both "initiate" and "carry" pain messages into the spinal cord
and up to the brain if they become irritated (386-388, 439).
ADVANCED: The pain pathways (how the pain gets from the disc to the brain) for
discogenic pain are still very controversial and may not function as traditional
anatomy has taught us. Traditionally, pain signals that originate in the nerve roots
adjacent to the disc or in the disc move from that root, into the corresponding
DRG and into the spinal cord. However, some new research suggests that pain
signals from the lower lumbar discs (L5 and L4) are (at least in part) detoured up

the sympathestic
nerves (i.e., gray
ramus
communicans)
and into the upper
lumbar DRGs especially at the
L2 level. (11, 259,
260) Clinically, in
some patients it
then would be
possible for
patients with L4
and L5 disc
problems to have
L1 or L2
dermatomal pain
(groin and anterior
thigh pain).

IDD: In a
Nut Shell:
When a Radial Annular (aka: anular - as they spell it in the UK) Tear enters the
outer 1/3 of the anulus, (Fig.#3) and exposes the sinuvertebral nerve-endings to
degenerated nuclear material (cytokines), pain may well occur secondary to
chemical irritation of these pain-carrying fibers. This type of pain is called
'Discogenic Pain,' which means that the pain arises from within the disc and
not the adjacent neural tissue. In Fig. #3 the disc has ripped through or
"disrupted" and has allowed nuclear material (pink) to escape into the outer and
sensitive 1/3 of disc. The sinuvertebral nerves (yellow dots) in contact with this
degenerated nuclear material have become inflammed (red dots) and irritated,
which inturn causes pain signals to 'firing' off pain signals to the dorsal horn of
the cord and then to the brain. Some patients even suffer a referred type pain
(discogenic sciatica) down the lower limb(s) from this condition, yet they
have no traditional compression of the adjacent nerve roots. [jump to tutorial]

HISTORY OF
INTERNAL
DISC
DISRUPTION:
(IDD)
IDD was first
described by
Crock in 1970 (8)
and again in 1986
(9). It was then
described as a
disruption' of the
internal
architecture of the
disc without signs
of disc protrusions
or without positive
signs for nerve
root
compression.
In his 1986 presidential address, Dr. H. V. Crock told members of the
international spine society that internal disruptions within the architecture of the
disc could result in back pain and even lower limb pain without the presence of
spinal nerve root compression (9). He termed this entity Internal Disc
Disruption or IDD.
In 1995, a 'Dream Team' of well respected and Volvo Winning researchers
(Schwarzer, Aprill, Derby, Bogduk) set out to test and further develop
Crocks theory of IDD and convincingly calculated the prevalence (frequency) of
IDD in patients with chronic low back pain. (2) The study also attempted to
determine if traditional examination findings and/or specific patient symptoms
could be predictive of the diagnosis of IDD. By following the strict criteria
specified by the International Society for the Study of Pain in its taxonomy (21),
these investigators calculated the prevalence of IDD to be between 30% and
50% with a 95% confidence limit. They also concluded that neither traditional
examination findings nor patient symptoms could predict whether or not a patient
had IDD. Unfortunately, it looks like provocation discography remains the only
way to confirm the diagnosis of IDD.
The theory of IDD as a source of chronic back pain is not without its critics. In
2003, Lee et al. reviewed the research on IDD from 1985 through 2000, (10)
although the papers review were mostly on radial tears, and HIZ. He summarized

that of the 13 research papers on IDD and similar topics, there was not much
agreement on what made the diagnosis of IDD. There was, however, some
general agreement between the groups on what constituted the diagnosis of
IDD: lower back pain, reproduced on provocative discography (concordant pain
was a strong indicator),and a normal neurological examination, i.e., no loss of
reflexes, no loss of muscle strength or atrophy, and no sensory loss. That's it,
only two factors! Other criteria for the diagnosis of IDD were not so universally
agreed upon were: the presents of an HIZ (high intensity zone) within the
posterior outermost region of the disc on the T2-weighted MRI, disc
degeneration, and a history of trauma.
Based on their review of '15 years worth of research', Lee et al. boldly concluded
that IDD is not real, but a hypothetical disease. This Korean group further
stated the following; Our personal view is that IDD is a doctor-made disease,
that is, an iatrogenic disc disorder, which may lead to an unconventional
invasive operations (referring to the IDET procedure and Lumbar
Fusion). (10) Lee felt that because the diagnosis was so dependent upon the
'subjective input' from the patient, during discography, that the diagnosis should
be thrown out!
IMHO: Lee, who is way out of his usual area of research on this
subject, is going to get 'blasted' for making such aggressive statements against
the theory of IDD, which has been accepted by the 'North American Spine
Society' (21) and 'International

Society for the Study

of Pain in its Taxonomy ' (21)! For the typical non-mentally

compromised chronic pain patient, the diagnosis of IDD can be made with a
reasonably degree of medical certainty by using the criteria that the International
Society for the Study of Pain in its Taxonomy have adopted (Here) for the criteria.
THE RESEARCH:
Although controversial (436), discogenic pain secondary to IDD is thought to be
responsible for a substantial number of chronic back and leg pain cases where
obvious nerve root compression is absent/lacking (132,2). In fact the famous
multi-time Volvo Award Winning author, professor Nikolai Bogduk MD, believes
IDD is the "most common cause of chronic low back pain" (1,2) and may be often
over-looked by the treating physician." (132).
Quality scientific research has demonstrated that 40% of all chronic back pain
is caused by the radial annular tears of IDD (2), and often presents (62% of the
time according to Ohnmeiss et al.) as back pain and/or pain down the lower
extremity, i.e., sciatica (6).

The exact mechanisms of discogenic pain are still controversial; however, the
development of a full thickness Radial Annular Tear that leaks nuclear material
(cytokines) into the outer annulus is most certainly involved in this syndrome.
This annular disc leak theory has been confirmed scientifically via numerous
quality peer-review investigations (105,115,116,123,124,131).
Recently, it has been demonstrated that IDD was the causative factor in about
three-quarters of severely acute nonspecific low back pain patients. More
explicitly, in 2005 Hyodo et al (16) performed MRIs and discography on 55
patients who all suffered severe, immobilizing, non-specific low back pain without
sign of neurological deficit. In 73% of these patients, a full thickness nonepidurally leaking annular tear was identified on discography that responded to
fluoroscopic lidocaine irrigation (a powerful anesthetic) by instantly 'stopping'
the patient's perception of severe pain. (16) The aforementioned experiment
strongly advocates that full thickness annular tears or IDD are a major cause
of severe acute non-specific low back pain.

THE DIAGNOSIS: Discography & GadoliniumDTPA Enhanced MRI

The 'International Society for the Study of Pain in its taxonomy (21) has adapted
the following set of criteria for diagnosing IDD: ) no visible disc herniations may
be seen on MRI or CT; ) during provocation discography injection of the
suspect disc with contrast, a recreation of patients 'exact' back and/or leg pain
must occur (353,9); injection the disc above or below the suspect disc must be
non-painful; this acts acts as a 'control disc' or normal disc; and a grade 3 or
4 radial anular fissure must be demonstrated on CT discography
(2,351,352,355).

Provocation discography, which may actually further damage the

disc, should ONLY be attempted if the chronic pain patient can
no longer live with their pain syndrome and is contemplating
IDET, SED, DiscTRODE, interbody spinal fusion or ADR.
Furthermore, their Oswestry better be at least a 50! (Oswestry)

The 'Gold Standard' in making the

diagnosis of IDD is a very painful
and invasive test called
'Provocation Discography' with
follow-up CT discogram. There are
two components to provocation
discography: the first is an attempt
by the doctor to 'provoke' or 'cause'
the patient to feel their 'usual' pain
(concordant pain) by pressurizing
the disc with a contrast material.
Note: in Fig.#6 the center of the
disc is being filled with contrast
material (white). If you look closely,
you can see the fine 'white' needle
(black arrows) entering the posterior
of the disc. This (fig. #6) represents a normal disc that 'holds' the dye within the
nucleus and does not demonstrate any anular tearing.

Fig.#7, on the other hand, demonstrates two completely

disrupted discs: The contrast material (black in this photo) has
NOT been contained within the center (nucleus) of the disc. This
time, it has clearly leaked through internal 'disruptions' within the
posterior anului of the L4/5 and L5/S1 disc. In fact, the L4/5 disc
has been completely disrupted and it leaking contrast material
directly into the epidural space (black arrow). The latter situation
is called a Grade 5 anular tear or Grade 5 IDD. (learn about the
dallas discogram naming system and the different degrees of
disc disruption here about half way down the page.) This
situation may indicate big trouble, especially if you are one of
unfortunates who are 'sensitive' (allergic) to those leaking
biochemicals (cytokines), for the delicate posterior neural
structures 'dwell' adjacent to the posterior of the disc and may
become inflamed and/or damaged from this leakage. More
explicitly, substance like TNF-alpha, IL-1, IL-6, NO,
Phospholipase A1 may stimulate some form of 'attack' within the
nerve root and ultimately lead to permanent nerve (axon) death.
Neuropathic pain may be spawned.

MRI Identification:
Gadolinium-DTPA
Enhanced MRI
Although provocation
discography with CT
discography is the "gold
standard" when it comes to
making the diagnosis of
symptomatic IDD, the
procedure itself can inflict
damage upon the disc and
"spawn" degenerative disc
disease (30-34,530). As an
alternative, the use of
gadolinium (contrast)
enhancement may be
considered. GadoliniumDTPA, which is injected into the blood stream during the MRI,
will "light-up" the granulation tissue that forms within a
healing/healed full thickness annular disc tear.
Fig.# 9: The MRI images to the left demonstrates how
gadolinium will "light-up" a healed anular tear. Note the L4 disc
shows no sign of posterior disc tearing (black arrow); however,
after the administration of gadolinium during the MRI, the same
T1 image demonstrates the remains of the massive annular tear
(red arrow) I suffered back in 2002.

The gadolinium also high-lights continued swelling/granulation

tissue within my L5 disc over 1 year post micro-discectomy. No
disc herniations are noted.
The HIZ phenomenon also give us a clue that Internal Disc
Disruption might be involved in the patients pain syndrome
although this T2-weighted MRI finding is highly controversial. For
more information, visit my HIZ page.

The IDD Tutorial:

To begin this tutorial, lets look at what a normal disc looks like
from the over-head view (axial):
In Figure #1, the basic anatomy of the disc is shown: First note
the gelatinous and hydrated nucleus pulposus (#1 pink) that is
corralled (held in place) by a tough and fibrous anulus fibrosus
(#2 green). To give the anulus fibrosis, which is like the tread of a
tire, extra support posteriorly, the posterior longitudinal ligament
or PLL (#7 blue) exists and is tightly bound to the outer fibers of
the anulus. Also note the posterior neural structures: #10 (motor
& sensory nerve roots), #3 (mixed spinal nerve roots), and red

star (free-hanging nerve roots within the cauda equina). It is

these delicate neural structures that often become damaged and
perpetually generate
pain. To learn more
about spinal anatomy,
go 'here'.
It is extremely
important to
understand that, unlike
the rest of the
avascular disc, the
outer 1/3 of the anulus
fibrosus, the cauda
equina (red star) and
the PLL (blue #7) are
innervated with (full of)
tiny nociceptive Cfibers (pain carrying
nerve fiber) that, if irritated, have the potential to cause severe
PAIN and DISABILITY within the patient (4,55,56).

THE BIRTH OF INTERNAL DISC DISRUPTION:

The first step in the IDD process is for the disc to first degenerate
(lose water content and become brittle) and then (usually
because of trauma to the back or neck) tear open from the inside
out, or, sometimes, from the outside in (30-34,530). Ironically,
however, it seems that IDD can both 'cause' disc degeneration or
result from its presents. (5) The disc in figure #2 shows what is
commonly called Degenerative Disc Disease (DDD). DDD,
which can only be seen on T2-weighted MRI that will affect the
disc by causing a loss of water content, which in turn causes the
disc to become brittle and prone to tearing. In Figure #2.,
which represents a Grade IV Radial Anular Tear, our disc has
obviously changed in appearance when compared to Figure #1
and now demonstrates disc desiccation (dark green

appearance), bulging (note how the posterior of the disc is no

longer concave and has bulged into the nerve roots), and a fullthickness radial anular tear (red arrow) that has allowed nuclear
material (pink) to come in contact with the ultra-sensitive
sinuvertebral nerve-endings (yellow poke-a-dots). For some of
us, this situation is truly disastrous! Full thickness radial anular
tears, however, (red arrow) are not the only anular sign of the
degeneration process: concentric anular tears (white arrows) and
rim lesions - which also may result in severe back pain - are also
often present in the pathologically degenerated discs and may
also eventually spawn the deadly, disc-extrusion-producing, fullthickness radial tear (30-34). Note in Figure #2, the sinuvertebral
nerve-endings adjacent to the anular tear have become inflamed
(red), pissed-off, and are sending pain signals up to the brain
through both
the
sympathetics
(gray ramus)
and the
same-level
afferent nerve
roots.
In figure #7,
the situation
has worsened
into the
grade V
radial anular
tear (ship's
anchor). This
massive
disruption,
which may or may not be 'leaking' nuclear material upon the
adjacent nerve roots, is irritating even more sinuvertebral nerveendings and is probably resulting in much more patient pain and
suffering and even may cause referred pain down the back of the

leg (fake
sciatica, or
discogenic
sciatica) that
mimics
sciatica (6,7).
The pain
mechanism of
IDD not only
comes from
irritation of
the nowexposed
sinuvertebral
nerve
endings: a
the second
mechanism of
pain my occur from mechanically pressure upon these nerve
endings.
To make a long and complex explanation short: because of the
massive anular disruption (red arrow), the inside of the disc
(nucleus pulposus - pink) can no longer support the weight of the
body and 'shifts' this axial load outward onto the already
irritated and pissed-off posterior anulus. This added mechanical
pressure, like squeezing a cut finger, further irritates the
sinuvertebral nerve roots and create even more back and
possible leg pain. Remember, this condition, which may or may
not show up on MRI, will affect about 40% of all chronic back
pain sufferers and often requires surgical decompression via
fusion.
As if things aren't bad enough, let's meet the dreaded Grade V
Full Thickness Anular Tear:
Figure #8, depicts such a condition: Not only is the disrupted
disc generating back (discogenic pain) and possibly leg pain

(discogenic sciatica), but now we have the potential for the

posterior neural structures (traversing nerve roots, exiting nerve
roots, and dura of the thecal sac) to become irritated, inflamed,
and even killed! This condition, which I'm probably the proud
owner of, may baffle even the most astute doctor, by causing a
full blown, EMG-confirmed, radiculopathy WITHOUT the
presence of any sign of the classic nerve root compression!
Here's how it may work: The leakage of degenerated nuclear
material from crack(s) that have sprung in the final layers of the
anulus fibrosis of the disc will soak the delicate nerve roots
(which make up the sciatic nerve) with degenerated nuclear
material that is filled with all sorts of potentially inflammatory and
irritating biochemicals (TNF-alpha, NO, PLA-2,
Metalloproteinases, IL-6, PGE-2, Substance-P, Calcitonin generelated peptide). Although the exact mechanism is of this
Chemical Radiculopathy is unknown, it undoubtedly
involves the formation nerve root inflammation, intraneural
edema formation, and ultimately intraneural fibrosis (287).
OR, in layman's terms: stuff leaks out from the back of the disc
and damages (often permanently) the nerve roots that make up
the giant sciatic never that courses from the low back down the
back/side of the lower limb. We experience this nerve damage
as PAIN in the back and down the leg - sciatica.

TREATMENT OPTIONS:
Warning: These recommendations are for Educational Purposes ONLY and
should never be substituted nor take the place of an examination or
treatment plan by your own medical doctor! Do NOT implement any of these
courses of treatment without the approval of your medical doctor.
IDD is a very, very tough condition to treat, especially since the diagnosis is fairly
controversial to begin with and many primary doctors have never even heard of
it. Conservative care is ALWAYS the first form of treatment! If this fails then
provocation discography is indicated before proceeding to the more aggressive
treatment options but your Oswestry should be in the 50s. Here are the current
(7-28-04) treatment options available of IDD:

TREATMENT OPTIONS FOR IDD (in order)

Around 90% of all IDD sufferers will obtain satisfactory

relief from their pains by just hanging in there and using
conservative measures. However, it's very easy for the
patient to become frustrated by the fact that IDD often
takes many months (18 month on average) to heal. I
would NEVER recommend a patient rushing into a
decompressive fusion (or even SED) until they have
waited at least 18 months (preferably 24 month) unless
Conservative serious medical complication occur (loss of bowl &
bladder control, progressive neurological deficit, or
Care,
Medication & severe intractable pain). Conservative treatment option
Mother Nature: include the following: Medication, Gentle Traction
treatments (via RPT or Chiropractor), VAX-D (if you can
afford it), and non-dynamic spinal stabilization
training/exercise (maybe swimming). The worst thing to
do is just sit around and do nothing! Try and stay as
active as possible without severely flaring yourself up.
Figure out a way to get that heart rate up in an aerobic
zone to enhance blood flow to the disc, which should
help with the healing process.

Intradiscal
Injection:

Although this is still considered a 'fringe', there is now

some anecdotal evidence that injecting a 'chemical
soup' into the disc (and facets) may have some benefit
for pain relief in the chronically disabled (13). This
chemical soup includes the following: Chondroitin
Sulfate, Glucosamine Hydrochloride, DMSO, Marcaine,
dextrose (50% of the mix!). This chemical soup is
injected under fluoroscopy directly into the disc and
facet joints. A pilot study demonstrated that 57% of a
group of long-time chronic pain sufferer got about a 74%
decrease in both their disability scores and their pain
levels. However, PLEASE remember that this was a
very small pilot study that needs to be followed up upon,
so the results although promising must be taken with a
'grain of salt.' There were lots of 'problems' with the
study which I've commented upon in my review of this
paper. (Here: Klein, Mooney, Derby et al.)

SED (selective endoscopic discectomy) was created by the innovative Dr.

Anthony Yeung MD who uses an endoscope to enter the disc
(transforaminally or intralaminally), look around, and repair anular tears. The
beauty of this technique is that he is not bound by the limitations of
fluoroscopy, which may cause improper placement of any tear-sealing
device, for he can physically 'see' inside of the disc and anular tear; this
insures exact placement of the RF probe and/or laser.

Selective
Endoscopic
Discectomy
(SED):

Radio Frequency
Annuloplasty:
(discTRODE)

You can think of this technique as an 'eyeball-guided' debridement of a

damaged disc which is followed by an attempt to destroy granulation tissue
and inflammatory tissue within and round the anular tear. He, thankfully,
does NOT use IDET technology to perform the annuloplasty, but rather uses
specifically directed RF energy to accomplish the task of ridding the disc of
pain-producing tissue in and around the anular tear. Any nuclear fragment
within the tear (which are the precursors to disc herniation) are removed.
WARNING: Although this procedure has a good 'self-proclaimed' track
record, the doctor still refuses to put his procedure to the ultimate test: a
double blind investigation where it's compared with traditional discectomy,
IDET, and Sham treatment. Because of this, I CAN NOT INCLUDE
ENDOSCOPIC SYLYE DISCECTOMY FOR THE TREATMENT OF
COMPRESSIVE DISC HERNIATIONS AND EXTRUSIONS that result in
radicular pain. However, I think the treatment makes a lot of sense for the
treatment of IDD and eventually will be proven to be as effective for
decompression as traditional discectomy. Another downfall is cost. Although
I'm not 100% sure, I've heard that this procedure costs between $15,000 to
$25,000.00 which insurance may or may not cover? I've recently reviewed
both of Dr. Yeung's Endoscopic Procedures: SED and ENDOSCOPIC
DISCECTOMY.

IDET, which 'indirectly' uses Radio Frequency (RF) to heat discal tissue, is NOT
what I'm recommending here. Annuloplasty preformed with disctrode technology (or
SED technology) uses RF energy to 'directly' heat the target discal tissue. The
cannulas (wires that are used to produce the heat) are more steerable (the doctor
has more control of where he places the cannula) and can generate a more
controlled form of heating in a more specific location. The goal of RF annuloplasty is
destroy pain producing tissue and nerve fiber within the annular tear, and encourage
the anular tear to heal. The biggest disadvantage is that the doctor must use
fluoroscopy to see where he's got the needle tip (which generates the heat which
'cooks' the evil IDD tissue). Although this method is better than nothing, it's not
nearly as accurate as the SED procedure.
Again, there are no double blind studies out on this technology, but I expect they will
be coming. IDET has had several negative investigations, and I have heard and
seen too many failures to recommend its use.

If all else fails, this is your last stop! ADR is now available in the US (one or two
levels) and is probably one of your best bets. Dynesis is still in clinical trials but looks
Artificial Disc
promising as well. Both of the aforementioned are probably better options than
Replacement (ADR)
(Prodisc & Flexicore): traditional interbody fusion since they not only decompress/remove the diseased
Dynesis:
Interbody Fusion:

disc, but they allow for the spine to retain some of its natural motion - which is
thought to lessen the chance of 'over-loading' the disc above and below the fusion
(the domino effect). I'll comment more on these three final options at a later date.
However, your Oswestry score had better be in the 50s before you attempt this
drastic of a procedure. The empirical success rates are only about 33% with another
33% getting worse and the final 33% staying the same.

General Info. | Treatment Options |The Tutorial | Disc

Bulge | Disc Protrusion | Disc Extrusion | Disc
Sequestration
In layman's terms, a disc herniation occurs when the inside of the
intervertebral disc (nucleus pulposus) tears its way through the
posterior outer portion of the disc (annulus fibrosus) and invades
the space where the delicate neural structures reside (i.e., the
anterior epidural space). The presents of this nuclear material in
the anterior epidural space may irritate these neural structures,
which in turn may cause the patient to suffer severe back and/or
leg pain. In this tutorial we will explore just how a disc herniation
occurs and discuss some of the more common classification of
herniation.
The term 'Disc Herniation' (or 'disc prolapse' as they use in
Europe) is a broad and general term that includes three specific
types of disc lesions, which are classified based on the degree of
disc disruption and posterior longitudinal ligament (PLL). The three
main classifications of disc herniation are Protrusion (aka:
contained herniation or sub-ligamentous herniation), Extrusion
(aka: non-contained herniation, or trans-ligamentous herniation)
and Sequestration (aka: free fragment). These terms will be
discussed more below.
Figure # 10, which is a sagittal (from the side view) T2 Weighted
MRI lumbar image, demonstrates two types of disc herniation: the
L5/S1 disc has suffered a 9mm disc extrusion (red arrow) that is

not contained by
the PLL. The L4/5
disc has suffered a
smaller 4mm disc
protrusion (green
arrow) that is
contained by the
PLL. The L3/4
(blue arrow) is
completely normal
and has no disc
material projecting
posteriorly into the
epidural space.
Also note that the
L3/4 disc is white
in color, which
indicates it is nondegenerated (i.e.,
full of water and
healthy
proteoglycan). The
two herniated discs
(L4/5 & L5/S1) are "black" on this MRI image, which indicates disc
desiccation (lack of water and proteoglycan) and is termed
"degenerative disc disease" (DDD), which is usually a precursor to
disc herniation for it weakens the annulus which contains the
pressurized nuclear material.

General Information and Confusion:

In 1934 the syndrome of "disc herniation" was born when Mixter
and Barr first proclaimed that a posterior rupture of the
intervertebral disc that allowed nuclear material to escape and
compressed the adjacent spinal nerve root(s) was a common
cause of back and leg pain - sciatica (125). For nearly 70 years this
assertion has held true without much challenge(170).

However, modern research as demonstrated that the relationship

between disc herniation and its often associated sciatica are a far
more complex and bewildering phenomenon than once realized.
For example, since the invent of MRI, we have learned that some
patients have disc herniation on MRI, yet have no pain at. And,
visa versa, some patients have terrible back and leg pain, yet have
no disc herniation! (Click here for the false positive rates for MRI.)
Moreover, when post MRI is performed on some patients that once
suffered disc herniation induced back and leg pain, the herniation
is still there, yet the patient is gone. Conversely, some patients who
fail to recover from back and leg pain, demonstrate a
disappearance of the once prominent disc herniation.
Other ironies of disc herniation have been discovered as well. For
example, we have learned from the work of Karppinen et al. that
the size and severity of disc herniation do NOT correlate with the
degree of patient pain, disability, or suffering (170). That is, small
disc herniations and even disc bulges may causes just as much
pain and disability as massive disc herniations and even extrusion.
Another strange irony is the fact that smaller, less complete, and
innocent looking disc herniations (i.e., contained herniations,
protrusions and/or disc bulges) are usually more difficult to treat
and respond less favorably to decompressive surgery (discectomy)
than do the larger and more advanced disc extrusions and
sequestrations. (50) Moreover, symptomatic contained
herniations have a poorer prognosis for recovery than do the larger
more complete disc extrusions and sequestrations do. (50) And, to
further cloud the water, we now know that sciatica (a horrible
burning lower limb pain associated with disc herniation) is not
always causes by the direct pressure from a herniated disc. That
is, it can be caused from nuclear material "leaking" from the back
of the disc onto the adjacent nerve roots, i.e., chemical
radiculopathy(3,4) and/or from chemical and pressure irritation
of the posterior intradiscal nerve fiber, i.e., the sinuvertebral nerves,
which is called discogenic sciatica (1,2).

So, diagnosing a patient with complaints of back and lower limb

pain is certainly not as easy as once believed.

TREATMENT OPTIONS: SURGERY VERSUS

CONSERVATIVE CARE
Based on nearly thirty years of medical research, I can comfortably
conclude the forthcoming with respect to treatment options for disc
herniation induced back and lower limb pain: for patients who do
not have the danger signs of compressive disc herniation--i.e., loss
of bowl and/or bladder control (cauda equina syndrome);
progressive worsening of their neurological state (atrophying
muscles, progressive muscle weakness [foot drop]); and/or a
worsening of their pain--conservative, non-operative care,
will work just as well as having back surgery. In 1982,
Weber--who won the prestigious Volvo Award for this work--was
the first to suggested that back surgery for disc herniation induced
back and leg pain was no more effective than letting old man time
and mother nature (i.e., having conservative care [i.e., physical
therapy, exercise and physical therapy]) work their magic. That is,
he experimentally demonstrated that in the long run, patient who
had back surgery got no better than those who didn't. The surgery
group, however, did get better faster and were doing better at the
one year mark; however, by three years, there were no differences
between the surgery group and the non-surgery group. [Weber
Study] Other investigators have confirms these findings. Recently
(2007) Peul et al published the results of their medical investigation
into surgical outcome of sciatica in the prestigious New England
Journal of Medicine. They also randomized over 200 patients into
either a disc surgery group or a conservative care (non-surgical)
group. Again, as with the Weber study, the patient who had surgery
got rid of their leg pain faster; however, at the one year follow-up,
the surgical patients were no better off than that of the non-surgical
patients. [An abstract of the study is here]
DISCECTOMY:

Treatment for severely symptomatic disc herniation-associate

sciatica is best accomplished with traditional open discectomy or
micro discectomy (99), BUT ONLY IF conservative measures have
failed and/or if you have the danger signs associated with disc
herniation: loss of bowl and/or bladder control (cauda equina
syndrome); progressive worsening of the neurological state (rootrelated atrophying muscles, progressive muscle weakness [foot
drop]); absent reflexes and/or a worsening of pain. Surgery timing,
for disc herniation-related sciatica, is also critical. That is, you
certainly don't want to wait any longer than one year before having
the surgery (50). See the Surgery Timing Page for more
information.
ENDOSCOPIC & LASER:
With regard to the non-invasive techniques, such as endoscopic
discectomy, laser discectomy, etc. I'm not a believer and I
do not recommend them. With regard to Laser discectomy,
neither does a 2007 meta-analysis (a study of all the research ever
done on Laser discectomy) by Goupille et al (26) who state, "this
treatment cannot be considered validated for disc herniationassociated radiculopathy resistant to medical treatment." Until the
inventors and proponents of these procedures step-up to the plate
and published some high quality medical investigations (like what
Peul et al just did) to prove their efficacy (effectiveness), then I'm
not a believer. I can only think the reason the inventors of these
techniques haven't done so is because they are afraid that the
studies will show their techniques are no better than traditional
discectomy or even worse. SO, STEP AND SUBMIT YOUR
RANDOMIZED CONTROLLED TRAILS! PUT YOUR RESEARCH
WHERE YOUR MOUTHS ARE!

THE TUTORIAL: THE BIRTH OF A DISC

HERNIATION
Lets begin our tutorial with a quick review of the normal disc, and
then proceed through each type of herniation. (For a full review of

disc anatomy and physiology, please visit my 'Disc Anatomy

Page'.)

The Normal
Disc:
Figure #1: The
'Nucleus
Pulposus' (pink
#1), which is a
water-rich gel-like
mass of
proteoglycan
material, has the
duty to support the
tremendous 'AxialLoad' (weight) of
the body. This
nucleus is
'corralled' by the
stronger 'Annulus
Fibrosus' (green
#2). The annulus is
made out of
concentric rings of a cartilage-like material called 'lamellae' (#9). It is this
specially arranged collagen that gives the annulus the tremendous strength
needed to hold that nucleus in place. Key Concept: The nucleus pulposus,
because of the tremendous axial load upon it, is constantly trying to escape from
the confines of the center of the disc. If it does manage to escape (tear) through
the PLL (#7), the appearance on MRI is called a disc extrusion. The
'Posterior Longitudinal Ligament' (PLL #7) shields the delicate
posterior neural structures and acts as a last line of defense against the
potentially irritating nucleus pulposus. Note the posterior disc is 'concave' in
shape, as outlined by the PLL. (It will not stay concaved for much longer!) The
'posterior neural structures', which are very sensitive to pressure and chemical
irritation, include the following: 'Spinal Nerve Roots' (L4, L5, S1), 'Dura Mater or
the Thecal Sac ' (red star), and the 'Dorsal Root Ganglion' (DRG). To learn
about the anatomy and physiology of the disc go to: [Disc Anatomy]. And finally
we have the Sinuvertebral Nerve (# SN). The Sinuvertebral nerve
innervates (connects to) the outer 1/3 of the annulus fibrosus. These tiny nerve
ending have the ability to carry PAIN messages to the brain and are thought to
be on of the causes of discogenic pain. (Read my IDD page, for more

information on discogenic pain.) Oh, one more thing; the epidural space (#8)
contains the traversing nerve roots (L5) that are often the favorite target
of the compressive disc herniation.

THE DISC BULGE: The First Step Toward Disc

Herniation:
In order for a disc to herniate, its structural components must first 'weaken'. This
weakening occurs as a result of Disc Degeneration. Disc degeneration occurs
naturally, to some degree, in all disc, but in some people the process become
especially severe and damaging. The 'bottom-line' of the degeneration process is
that the annulus becomes dried (desiccation) and brittle, hence allowing for the
development of Disc Bulging and full thickness posterior anular tearing, or
Internal Disc Disruption.
Figure #2 demonstrates the 'pre-cursor' to a disc herniation. This type of disc
lesion - that bulges into the anterior epidural space without any area of focal-ness
or out-pouching - would be called a 'Disc Bulge' on MRI (only because the
MRI can NOT show the condition within the disc), although in reality it is a
'Grade 3 Radial Anular Tear' (you would need CT discography to identify
the tear) that has disrupted the posterior annulus and allowed irritating nucleus
pulposus material to enter into the outer fibers of the disc. Again, this in of itself
(IDD) may cause severe and disabling pain in some unfortunate people;
however, the subject of Internal Disc Disruption is not the focus of this page. Also
note that the PLL, although bulged, continues to be intact and has not ruptured.
As well shall see later, the PLL is the 'key' to differentiating between a disc
protrusion and a disc extrusion. Finally, note that the Sinuvertebral nerves are
irritated (red) and are sending pain signals on to the brain through the
sympathetic nervous system (gray ramus communicans). Also note that this IDD
may cause some referred lower leg pain as well (spinal nerve has some orange
in it to indicate referred pain.)

DISC

PROTRUTION: Posterior Longitudinal Ligament is

still Intact.
Figure #3 demonstrates a 4 millimeter disc protrusion and represents a
worsening of our disc bulge. The posterior of the disc is 'focally' or 'eccentrically'
pushing backwards into the anterior epidural space and has contacted, and even
somewhat compressed, the traversing nerve root (white star) and right front
corner of the thecal sac. Note that the PLL (blue) still has NOT be disrupted and
is still "containing" the near-herniated nuclear material.

The type of
presentation in
Figure #2. would
be 'officially'
classified as a
'Disc Herniation'
or, more
explicitly, a Disc
Protrusion
(aka: contained
herniation or
subligamentous
disc herniation).
Although disc
protrusions are
seen in about
30% of the
normal nonsymptomatic
population, nerve
root compression is not, and if much more indicative of a 'problem. This patient
may well be suffering right sided radicular pain (sciatica) and/or lower back pain
as a result of compression/irritation of the traversing nerve root and/or irritation of
the sinuvertebral nerves in the posterior of the disc.

THE DISC EXTRUSION: The Posterior

Longitudinal Ligament has ruptured.
Figure #4. demonstrates a more serious progression of our pathologically
degenerated disc: An 8 millimeter Disc Extrusion (aka: non-contained
herniation, transligamentous herniation) is now present. The PLL (blue) has
finally been defeated and has completely ruptured, hence allowing for further
migration of the the nucleus pulposus into the anterior epidural space. Note the
marked displacement of the traversing nerve root (white star) AND the exiting
nerve root (green star) (which has now turned completely red with inflammation
and venous congestion - the precursors for Radiculopathy). This Disc Extrusion
is NOT typically seen in the asymptomatic person and is often an indication for
surgical decompression; the sooner the better IF you're NOT improving with
conservative care. Another interesting phenomenon about extrusions are the fact
that these larger disc lesions have a greater ability to be 'reabsorbed' by the
body! This 'shrinkage phenomenon' has been demonstrated time and time
again in the literature; in fact, you can expect that in 80% of large disc extrusions,
there will be at least a 50% 'shrinkage' of size (5,6). Unfortunately, this doesn't
always mean that the pain associated with the extrusion will fade! Some patients

recover from disc extrusion yet demonstrate NO change in the size of their
extrusion at all, where others fail to recover yet their extrusion has markedly
decreased in
size! That just
goes to prove
that we still have
a lot to learn
about the
relationship
between disc
herniation and
pain!

DISC

SEQUESTRATION: The Final End-Phase of the

Disc Herniation.
Figure #5. represents the end-of-the-line for the cycle of disc herniation. Now we
can see that a big 'chunk' or 'fragment' of nuclear material has detached itself
from the main body of the extrusion is and loose in the epidural space. Note the
resulting severe compression of the traversing nerve root (white star), the exiting
nerve root (green star) and the lateral aspect of the Thecal Sac (blue star).

Sequestration (aka: sequester, free-fragment) may be excruciatingly painful

(back and leg pain - sciatica) and, if centrally located, may occasionally cause
the patient to lose control of their bowl and bladder function, i.e., Cauda Equina
Syndrome, which is considered a 'Medical Emergency'!
As with the disc extrusion, the sequestration may also undergo a reduction in
size from a combination of an immune attack {macrophage attack} and
dehydration, although frequently the patient will need immediate decompressive
surgery to beat this monster!
MRI DISC HERNATIONS: Some real pictures.
Figure #6. demonstrates a large 9mm disc extrusion (red star) as visualized on
both the Axial (over-head) and Sagittal (side) views.

Note that this extrusion has completely blotted out (can't see) the right traversing
S1 nerve roots (left side of image) and has pinched it against the lamina (tiny
green arrow). Note the thecal sac is moderately to severely compressed by this
large herniation, as noted on both the axial and sagittal images (between blue
arrow and red star).
This young man (24 years) has avoid surgery and is doing fairly well, although
his days of heavy work are probably over for good.

[ | The Normal Disc | Three face of Disc Bulge | MRI

Presentations | ]

Introduction:

Of all the e-mail

questions that I
received, the
question "What
is a disc bulge
and can it
cause pain?", is
by far the most
common.
The answer to
this question is
not as 'black &
white' as many
doctors will
have you
believe.
Although about
80% of completely asymptomatic people will demonstrate a disc
bulging or worse on MRI (1-4) (MRI False Positives), about 40% of
chronic back and/or leg pain patients will have 'disruptions' (tears)
within the substance of their discs that are often invisible on MRI.
(5) Fig.#1 depicts such an 'internal disruption'. Note that the
posterior of the disc has bulged into and contacted the anterior
portion of the thecal sac (dura & arachnoid mater) - your typical
disc bulge. What the MRI may not demonstrate is the wide full
thickness 'Radial Anular Tear' that connects the Nucleus with
the outer layers of the anulus. Note that the Sinuvertebral
Nerves, which have been exposed to the irritating nuclear
material, are irritated (red dots) and generating chronic back pain.
Although I've covered IDD ad nauseum (here), I think it best that
we touch on this important subject here as well:
Internal Disc Disruption (AKA: IDD): IDD, which is
believed to be a major cause of 'discogenic back pain' (5,6), occurs

when the intervertebral disc develops a 'rent' or 'tear' through its

substance. This tear, because of the high pressure within the
nucleus, allows the irritating nuclear material to escape the
confines of the nucleus pulposus and enter the nerve infested
outer 1/3 of the anulus fibrosus. It is believed that, in some
patients, an inflammatory reaction can occurs within that outer 1/3
of the anulus, hence causing chronic and debilitating back pain
and/or leg pain (5-10).
The Birth of a Disc Bulge: The Normal Disc.
Lets do a quick refresher course on normal disc anatomy: (click
'here' for a more thorough lesion.)
We shall study the evolution of the 'disc bulge' from an over-head
vantage point (aka: axial views): The most important thing to keep
in mind is that in a normal, non-bulging, disc, the Ring Apophysis is
visible and NOT over-shadowed by a bulging anulus. Fig.#3
demonstrates this nicely: note that the posterior of the disc has a
concave configuration. and no disc material has bulged past the
posterior ring apophysis. I will now 'briefly' discuss the main
components of the disc. For a full discussion on disc anatomy see
my 'Disc Anatomy' page.
The Nucleus Pulposus (pink) is the gelatinous-like center of the
disc. Normally, is has a very high water content, as it is
predominantly composed of proteoglycan molecules produced by
the cells of the nucleus. It's job is to absorb the tremendous
downward weight of the body (like the shock absorber of a car) and
act as a pivot point to allow motion between the bones of the spine
(vertebrae).

The Anulus
Fibrosus
(green) is a
fibrous
structure that
surrounds the
nucleus and
shields the
delicate nerve
roots and
thecal sac
from the
irritative
nucleus
pulposus. It's
made up
mostly of
collagen
which is generated from fibroblast like cells. It has a much lower
water content than the nucleus. The anulus is a layered structure,
in that it contains 15 to 25 sheets of collagen; these sheets are
called Lamellae and are 'glued' together with proteoglycan
molecules. The job of the anulus is to corral the highly pressurized
nucleus and protect the highly nerve-infested outer 1/3 of the
anulus and posterior epidural neural structures.
The Sinuvertebral Nerves (yellow balls) are tiny nerve fibers and
endings that live in the posterior 1/3 of the anulus fibrosus. Irritation
of these pain-carrying fibers are thought to be one of the causes of
discogenic back and/or leg pain.
The Posterior Neural Structures (bigger yellow balls): Within the
anterior epidural space (black) lives the delicate spinal nerve roots
(NR), thecal sac, and exiting nerve roots (spinal nerve). It's
important to understand that at each disc level, there are two nerve
roots that are vulnerable to irritation: the 'Exiting Spinal Nerve
Root', and the 'Traversing Spinal Nerve'.

THE THREE FACES OF DISC BULGE:

Asymptomatic, Grade 3, and Grade5.
The Disc Bulge: Asymptomatic - (grade 1 IDD)
Figure. #4 depicts a 'Bulging' lumbar disc. Note that the posterior
of the disc has bulged backwards past the ring apophysis (gray)
and into the anterior epidural space. This bulge has slightly
contacted the left Traversing Nerve Root without pushing it out of
place (#2).
This is quite a
typical
presentation
for a disc
bulge; one
that your
doctor might
call
completely
normal!
Also note that
the disc has
greatly
degenerated
(dark green).
DDD is
usually a
precursor to bulging. You can learn more about DDD (degenerative
disc disease) on my DDD page, but to recap, DDD begins from
discal trauma and/or nutritional compromise. What ever the cause,
once it begins a vicious cycle is perpetuated that leads to discal
drying, weakening, and tearing. In fact, in our model to the left, the
disc has indeed began steps toward pathological degeneration. A
grade 1 radial anular tear has developed and is allowing nuclear
material into the inner region of the anulus. This would not be
expected to be painful, for it has not progressed into the outer 1/3
of the anulus - which is where the sensitive sinuvertebral nerves

are. This would NOT be visible on MRI; only CT discography would

denote the above tear.

The Painful Disc Bulge: Internal Disc Disruption (grade 3 IDD).

Now, our above model has taken a turn for the worse! The grade 1
anular tear has progressed into a grade 3 full thickness radial
anular tear. Note that the sinuvertebral nerve is now 'activated'
(red) and transmitting pain signals to the brain! This is called
'Discogenic Pain' and usually presents as lower back pain, but it
may also
present as a
referred pain
down the
lower limb we call the
latter
phenomenon
'Discogenic
Sciatica'.
Note that the
bulging has
NOT worsen,
yet the disc
has become
painful. MRI
probably
would NOT
demonstrate this anular tear! Only a test called 'Provocation
Discography' can confirm the presents of IDD. Please go to my
IDD tutorial for more information on Internal Disc Disruptions.
As noted above, about 40% of the chronically disabled will have
IDD. Please read the research paper that demonstrated this
commonly used number (here: Schwarzer AC, Aprill CN, Derby R,
Bogduk N )

The Painful Disc Bulge: The Leaking Anular Tear (grade 5 IDD)
Another condition, which again is somewhat controversial, is the
leaking anular tear. Some believe that grade 5 anular tears can
leak biochemicals and nuclear particle from the disc and actually
cause true radicular like symptoms (sciatica) WITHOUT the
physical compression of the nerve roots. This has been termed
'Chemical Radiculitis' (11,12). Again, I've got this more
thoroughly covered on my 'Sciatica page', but lets recap: It is
known that nucleus pulposus, in vitro, can cause severe
neurological damage to the nerve roots (13-17). Complete full
thickness, leaking, anular tears are commonly seen during
discography. Therefore, some anular tears that leak, will soak the
adjacent nerve roots with nucleus pulposus and other
biochemicals. This may MAY induce severe damage to the nerve
roots and result in true radicular pain (sciatica). I'm convinced this
happened to me as well... how else can you explain a three level
radiculopathy
(L4, L5, and
S1) with no
compression
of the L4 or L5
nerve roots?

Our disc
bulge, in
Fig.#6, is now
'hiding' a
leaking grade
5 anular disc
tear. This
patient will not
only will have
lower back
pain but may
have full
blown root-pain (sciatica) and neurological deficit as well. I think

the picture speaks for itself. Note that the dura, traversing nerve
root and exiting nerve root are extremely inflamed and irritated.

MRI EXAMPLES:
The key for identifying a disc bulge is that the entire posterior of the
disc has bulged backwards, in a subtle, general manner, as noted
above in figure #4. This greatly differs from a protrusion or
herniation, in that
the protrusion is a
more "focal" or
"eccentric" or a
'concentrated outpouching' of a
portion of the
posterior of the
disc.
Figure #5 is a
perfect example of
how a disc
herniation presents
itself on MRI. Here
we have a 4
millimeter central
contained
disc
herniation (#2).
Note the severely dehydrated disc (#1) where you can not even
see much of a nucleus. Also note the S1 roots (#4), and the cauda
equina (#3) are free and clear of the herniation. Luckily this patient
had a large neural canal which allow for this herniation.
To make things still more complicated, you can have bulges that
give rise to herniation's. My MRI is a perfect example of this. In
Figure #6 you can see my axial MRI. Note the broad based
bulge (#2) that extends below a line that I've drawn represents
where the back of the vertebra should be. The disc should NOT

extend beyond this line! If you 'hallucinate' enough you can see
where the small 3 or 4 mm herniation (#3) 'eccentrically' disrupts
the smooth out-pouching of the bulge. These are very hard for the
untrained eye to see, but you can surely see the difference
between the clear cut 4 mm herniation above (Fig. 5) and the 4mm
disguised herniation to the left (Fig. 6). Also note that unlike the S1
roots in Figure #5,
my left S1 root has
contacted by the
herniation and
pushed it ever so
slightly backwards.
As a bonus, you
can see a nice HIZ
sign just to the left
(9 o' clock) of
number 3 (not
marked). It looks
like a white bubble.
Its even more
pronounced on the
real T2. (This film
is a 'proton density
image'.)

MRI Hints for IDDs presents: The HIZ Finding.

IDD, which is not often seen on MRI, can cause extreme and
disabling back pain and be very difficult to treat. Occasionally, in
about 30% of patients, it can be seen on MRI and presents as a
'high intensity zone' (HIZ) in the outer posterior anular fibers
of the lumbar disc. Figure #2 demonstrates this 'HIZ sign (red
arrow) which appears as a white bubble in the back of this badly
desiccated L5 disc. Pathophysiologically, these are believed to be
a combination of at full thickness radial anular disc tear that has
merged with a large concentric anular tear. (see my pages on
anular disc tears for more information.) When HIZ findings are

present in a painful disc, there is a very high chance (over 90%)

that the disc is completely torn through. There remains fierce
debate over whether or not the HIZ is predictive of a 'concordantly
painful' disc on provocation
discography, which is the only
tool we have to confirm the
presents of IDD.
Let's take a look at what a disc
bulge is, how it develops, and
how IDD may appear within
the bulge.

Radial Tears | Rim

Lesions | Concentric Tears | HIZ Sign
Anular Disc Tears: General Information
Disc herniations are all born from internal disruptions or 'anular tears' within the
substance of the anulus. In layman's terms you could say that the discs rips from
the 'inside-out'. We have learned from the disc anatomy page that the outer 1/3
of the disc has pain carrying nerve fiber embedded with in it. Therefore, any
tearing into this outer 1/3 of the anulus has the potential to cause back pain and
lower limb pain. This type of pain is referred to as discogenic pain.

There are three types of anular tears

(aka: anullar fissures) that occur in the
human disc: The rim lesion, which is
a horizontal tearing of the very outer
fibers of the disc near their attachments
into the ring apophysis; the
concentric tear, which is a splitting
apart of the lamellae of the anulus in a
circumferential direction; and radial
tears, which are horizontal or obliquely
horizontal tears which begins within the
nucleus pulposus and progresses
outward toward the posterior periphery
of the disc. (See Figure #0)
I've went into great detail about each of
these types of anular tears. Just click on
one of the links at the top of the page to further learn about the different ways the
disc can tear.
Researchers agree that anular tears are of great clinical importance for they have
the capability of producing severe and debilitating back and leg pain by
themselves, without that disc rupturing into a herniation. Anular tears cause pain
by irritating the well innervated posterior 1/3 of the anulus. Thats right, we now
no that the disc does indeed have tiny nerve fibers embedded within the out
anulus and has the potential to generate pain (30). In fact research has shown
us that blood vessels and nerve fibers have been seen growing into the inner
anulus in 46% of chronic back pain patients, and even into the nucleus its self in
22% of the cases (31). Therefore the degenerated disc of a disc tear survivor
may always be somewhat painful because of this nerve fiber in growth.
Another important clinical potential of peripheral anular tears are their ability to
induce premature degeneration in the disc (5). Animal studies in the pig and
sheep have demonstrated that induced rim lesions lead to severe premature
degeneration of the disc, endplate, and facet joint in 100% of the tested discs.
This is unconfirmed in humans for it is unethical to induce peripheral tears in
humans, but since the discs of the pig and sheep are both amazingly similar to
that of the human disc, it is quite possible that rim lesions in human also will lead
to rapid premature disc, end-plate, and facet degeneration as well. (click here to
lean more on the rim lesion studies.)
Although even the most stubborn tear usually heals within 18 months,
occasionally the tear and/or disc degeneration is too severe for the disc to heal
on its own and surgery may become necessary: The IDET is designed to seal off
a leaking radial tear; the Nucleoplasty is designed to shrink the volume of the

disc which may be just enough to reduce a grade 5 radial tear and small
protrusion and free up any minor nerve root impingement; and the last resort is
the removal of the troublesome disc via fusion.
As we will learn in detail below, anular tears are not always seen on MRI, and
never seen on x-ray. The best way to visualize anular tears is on CT
Discography. A discogram is performed by injecting contract material into the
center of the disc, and then watching to see if the dye leaks from that center
along a radial tear. Figure #1 and #2 are examples of CT Discography. In Fig. #1
the injected dye (black) does not leak out of the nucleus. This is normal. Fig.#2
demonstrates a massive Grade 4 radial disc tear. Note how the contrast (black)
has leaked out from the center
of the disc through a massive
complete radial tear. (See the
Discography page for more
information.)
The other, less invasive way,
to confirm the presents of an
anular disc tear is by MRI.
High Intensity Zones
(HIZ) are very effective at
predicting the presents of a
grade 4 radial anular tear.
Research agrees that HIZ
(High Intensity Zone) is fairly
accurate at predicting the presents of an underlying anular tear. However a huge
debate still rages as to whether or not this HIZ sign is predictive of that disc being
a cause of the patients back pain. In Figure. # 3, My T2 weighted MRI is a prime
example of an HIZ (white arrow). Also note another type of tear (black arrow) that
Bogduk calls an LIZ (Low Intensity Zone). To increase the chances of seeing a
true anular tear on MRI, contrast (gadolinium) may be added. Researchers have
noted that gadolinium will 'light-up' full thickness tears because the contrast will
accumulate in the vascular granulation tissue with that tear (32). (read the whole
story on HIZ Here.) HIZ are thought to represent a combination tear; a compete
radial tear, that has joined either a concentric tear or a rim lesion. (I will explain
this much more in depth Here)

HISTORY:
Researchers have long known about tear
formation within the intervertebral disc.
These discal tears were first noted by
Schmorl and Junghanns back in 1932. By
1952, two of the three types of anular tear
were thoroughly described by Hirsch and
Schajowicz (1). They described
Concentric Tears, as crescentic or oval
cavities filled with fluid or mucoid material
between lamellae of the annulus, which
were the result of ruptures of the short
transverse fibers of the lamellae, which hold
the anular lamellae together. They also
described Radial Tears as fissures
extending from the surface of the anulus to
the nucleus. The third type of anular tear
was first described by 'Schmorl & Junghans'
in 1971(2). They described Transverse
anular tears (aka: rim lesions) as tears in
the very outer fibers of the disc (Sharpeys Fibers) near the insertion into the ring
apophysis. These fibers occurred in a horizontal pain, parallel to the end-plate.
Since these initial descriptions we have learned a lot more about anular tears as
they have been extensively studied both microscopically and macroscopically.
Famed researcher Barrie Vernon-Roberts, who has devoted over 25 years to the
investigation of anular tears and disc degeneration, has published several
papers on the subject in 1977, 1990, 1992, and final in 1997. To date his 1992
paper entitled Annular Tears & Disc Degeneration in the Lumbar Spine yields
one of the best descriptions of the three types of anular disc lesions yet written. I
will use his research frequently through out this page. (3)
There is one commonly quoted misconception that I constantly see throughout
the internet. It was a theory based on the work of another famous researcher
and author, William H. Kirkaldy-Willis. This theory stated that anular lesions were
all related to one another and that radial tears originated in the outer regions of
the annulus, beginning as anular rim lesions and/or concentric tears. The theory
concluded that these peripheral tear would coalesce and work their way
inward toward the nucleus (4). Osti & Vernon-Roberts won the 1990 Volvo
Award in Experimental Studies by shooting holes in Kirkaldy-Willis theory, but yet
it still lives on?? It is now clear that the three types of anular tears are separate
pathologies and that radial anular tears begin as clefts within a degenerated
nucleus pulposus and work their way outward toward the periphery and NOT
inward (5, 6). Although the sheep studies of the 1990's do support the idea an
induced rim lesion will ultimately work their way into the center of the disc and

give rise to concentric tears, there is no evidence that the deadly radical tears
begin in the periphery. We now know that radial tears begin in the nucleus as
'clefts' and progress outward, NOT inward.
Let us now dive deeper into each of the three types of anular disc tears.

Radial Tears | Rim Lesions | Concentric Tears |

HIZ Sign

Anatomy | Dermatome Connection | Dermatome Research | Dermatome Map | The

Causes | A Cure? | MRI False Positives | Treatment | The Odds | Risk Factors | Will I
Recover? | The Outcome Studies|

Thou cold sciatica, cripple our senators, that their limbs may halt as
lamely as their manners. William Shakespeare 1564.

As you can see from the

Shakespearian quote above,
sciatica has been torturing
mankind for hundreds if not
thousands of years. In fact, there
has even been biblical mention of
this disease! (6) I can certainly
attest to the horror, frustration, and
true evil of this awful affliction!
Sciatica is a term which refers to a
burning, stinging, and/or numbing
pain that is felt in the buttock,
thigh, leg, and/or foot; it may or
may not be associated with low
back pain.
In layman's terms, sciatica is
caused by a pinching and/or
irritation of one of the three lowest
lumbar nerve roots that make up
the giant sciatic nerve. Any
pinching / irritation of these
delicate nerve roots may not only
may cause lower back pain but
may also ignite the entire sciatica
nerve into a pain state!

Fig.#1 shows the general location of the giant sciatica nerve

(yellow) which is the thickest and longest nerve in the human body.
When this nerve gets aggravated (red), there is often a lot of pain
involved over a large portion of the body (the lower limb). Note that
there are three main 'spinal nerve roots' (within the lower back)
that leave the spine and blend together within the pelvis and form
the sciatic nerve. These are labeled L4, L5, and S1.
Not all lower extremity pain is classified as 'true sciatica': Sciatic pain may be
classified as radicular pain (true sciatica) - pain radiating from the low back,
past the knee, and into the dermatome (L4, L5, and/or S1) of the affected lumbar
nerve root; or as non-radicular pain - pain radiating in the lower limb in a
non-dermatomal pattern (29). Bogduk defines radicular pain as a burning and/or
numbing pain that presents in a band-like dermatomal pattern below the knee
(7).

Now, if you already know the anatomy and understand what dermatomes are,
you may jump over the anatomy lessons and continue here : The Causes of
Sciatica

QUICK ANATOMY LESSION: The Formation of the

Sciatic Nerve.
Fig.#2 Illustrates the anatomy of the origin of the sciatica nerve in greater detail;
the backs of the vertebrae (posterior ring) have been cut away in order to see
how the sciatic nerve is formed.

Spinal Nerve Roots : one

motor root and one sensory root,
leave the cauda equina and course
towards their respective
intervertebral foramen (IVF). As
they 'transverse' towards the IVF,
they come in close contact with the
posterior surface of the
intervertebral disc. Herniations of
the disc can directly compress the
passing spinal nerve root and cause
back pain and sciatica.
Within the IVF the two spinal nerve
roots blend into one larger nerve;
this nerve is now called the 'Spinal
Nerve'. The Spinal nerve quickly
splits into a 'Ventral Rami', and
'Dorsal Rami'. The Dorsal Rami
courses to the skin and muscle of the lower back and butt, the Ventral Rami
courses downward to form the Sciatica nerve.
The only thing you really need to understand is that the L4, L5, and S1 Spinal
Nerve Roots make up the sciatica nerve. Irritation to anyone of these nerve roots
may ignite sciatica. For a better lesson and picture of real nerve roots, go to my
'Disc Anatomy' page and click the tab 'Real Nerve Anatomy'.

DERMATOMES & RADICULAR PAIN: Which Flavor

of Sciatica do you have?
The first order of business is to clear-up some terminology issues: The terms
Sciatica, Radicular Pain, Radiculopathy, Radiculopathic Pain,

and Root Pain are all synonymous (mean the same). I prefer the term
'Radicular Pain' since it more accurately denotes that the patients 'pain' is coming
from the spinal root level ('radic' indicates spinal nerve root) as opposed to a
referred pain from a facet joint, SI joint, or other spinal structure. The term
'sciatica' is not very specific and only indicates that the patient has lower limb
pain, which may or may not be caused from nerve root compression/irritation.
Since there are three possible nerve roots to irritate, and each of these nerve
roots are connected to different regions of the 'skin' (sensory) and 'muscle'
(motor) in the lower limbs, sciatica come in 'three different flavors': S1
radicular pain, L5 radicular pain, or L4 radicular pain (fairly rare).
L3, L2, and L1 radicular pains (aka: radiculopathy) are also possible with high
lumbar disc herniations; however, since these are not nearly as common and
DON'T involve the sciatic nerve, they will not be discussed here.

Dermatome Research:
Did you know that most of the dermatome charts floating around the internet and
on the walls of doctors' offices were based on investigations made over 35 years
ago at best (31), and over 90 years ago at worst (30). Heck, some investigation
date back to the 1800s (32)! Although in 1948 Keegan et al. had the right idea for
developing dermatome charts (33), in that he studies and mapped the effects of
disc herniations on the skin in the extremities, his results still couldn't confirm any
of the prior work!
Nitta et al: Finally, Nitta et al. published the first investigation that was of high
scientific design (2)! In 1992, this group of investigators successfully mapped the
sensory-dermatomal distribution of the L4, L5, and S1 nerve roots. They
gathered 71 patients, who were suffering disc herniation-associated radicular
pain, and 'blocked' (anesthetized) their problematic nerve root with Xylocain; this
was done under fluoroscopy to ensure the correct nerve roots were blocked.
Next they carefully marked (aka: mapped) the areas on the patients skin that
were numbed by the Xylocain nerve blocks. The results were tabulated and are
shown below; however, the bottom line is this: "The L4 nerve root innervates
(connects, gives-life-to) the medial side (inside) of the lower leg in 88% of the
patients tested. The L5 nerve root innervates the side of the first digit (big toe) on
the dorsum (top) of the foot in 82% of the patients. The S1 nerve root innervates
the side of the fifth digit of the foot in 83% of the individuals." (2) I've based all of
my dermatome maps on this investigation. (see below)
Although the majority of patients seem to share the same 'nerve root dermatomal
distributions' (wiring), this investigation has clearly demonstrated that the neural
anatomy of the lumbar spine does have some degree of variation, i.e., some 20%
of the patients did NOT have the typical 'nerve root dermatomal distributions'. For

example, in some patients, a L5 nerve root block would result in numbness of the
S1 dermatome and not the anticipated L5 dermatome (2).
Kortelainen et al: In another giant study of radicular pain patterns,
Kortelainen et al. also found that spinal nerve root irritation (via disc herniation)
did NOT always project pain into the classic dermatomal regions; this was
especially true of the S1 dermatome (1). After studying the radicular pain patterns
of 403 disc herniation-induced radicular pain patients - all of whom eventually
underwent discectomy surgery - they found the following:

Level of disc Number of

rupture
patients

L4 Dermatome

L5 Dermatome

S1 Dermatome

No specific
dermatome

L2 Disc

3 (0.7%)

(0%)

1 (0.6%)

2 (1%)

L3 Disc

7 (1.7%)

1 (9%)

3 (1.8%)

3 (1.5%)

L4 Disc

229 (57%)

7 (64%)

136 (79%)

66 (34%)

20 (74%)

L5 Disc

164 (41%)

3 (27%)

31 (18%)

123 (63%)

7 (26%)

403

11 (3%)

171 (42%)

194 (48%)

27 (7%)

Total

In summary, sciatic pain projection into the L5 dermatome (top of the foot) was
caused by the anticipated L4 disc herniation in 79% of the cases; by the
unexpected L5 disc herniation in 18% of the cases; and by the really unexpected
L3 disc herniation in 1.8% of the cases.
Pain project in into the S1 dermatome was caused by the anticipated L5 disc
herniation in only 63% of the cases, and by a unexpected L4 disc herniation in
34% of the cases! As you can see by these results, S1 dermatomal pain (pain on
the side of the foot) is not very accurate at predicting the level of nerve root
compression/irritation (1) (I would note that the Kortelainen study was not as

'scientific' as the Nitta study, and we can only assume that the disc

herniations all caused compression of the descending nerve root and NOT
the transcending root. There was no mention of this very important factor in
the paper!)
So, I hope I didn't loose too many of you in that last discussion! The bottom line
is that you can't always trust the presence of pain in a dermatome to indicate
which disc has herniated in the spine, although its still a moderately accurate
method.
Let's go over where patients typically feel nerve root pain.

Dermatome Mapping:
Without question, Nitta et al. has published the highest quality investigation on
dermatomes (2); therefore, only his work will be reflected on the following
dermatome maps:
S1 RADICULAR PAIN:
If the L5 disc herniates into the 'lateral recess' (which is where it usually does)
and compresses / irritates the descending S1 nerve root, the patient may suffer
an S1 radicular pain (aka: S1 root-pain, or S1 Sciatica). Fig.#4 shows the
regions in the lower limb where the patient will most likely suffer the symptoms of
S1 sciatica (2). As you can see, the majority of patients (75%) suffer the burning,
stinging, and numbing pain of sciatica in the lateral foot, posterolateral leg, thigh,
and butt, as well as, the bottom, outer 1/2 of the foot. These pains are the result
of damage and irritation to the 'sensory portion' (portion of the nerve root which
connects to skin) of the nerve root.

If the 'motor portion' (portion of the nerve

root which connects to muscle) of the S1
nerve root is damaged or irritated by the
disc herniation, the patient my suffer
weakness and/or atrophy in the
Gastrocnemius muscle (the calf), the
peroneal muscles (foot evertors), and/or
the muscles which flex or curl the 'big
toe'. The Achilles' Reflex and Plantar
Reflex may also be diminished or
absent. If severe, the patient will be
unable to do 'calf raises' with the
effected foot. Calf raising is the 'gold
standard' muscle test for S1.
L5 RADICULAR PAIN:
If the L4 disc herniates into the 'lateral
recess' (which is where it usually does)
and compresses / irritates the
descending L5 nerve root, the patient
may suffer an L5 radicular pain (aka:
L5 root-pain, or L5 Sciatica). Fig. # 5 shows the regions in the lower limb where
the patient will most likely suffer the symptoms of L5 sciatica (2). As you can see,
the majority of patients (75%) suffer the burning, stinging, and numbing pain of
sciatica in the top and inner surface (dorsum) of the foot, the outer-front of the
leg, and the bottom of the big toe. These pains are the result of damage and
irritation to the 'sensory portion' (portion of the nerve root which connects to skin)
of the nerve root.

If the 'motor portion' (portion of the

nerve root which connects to muscle) of
the L5 nerve root is damaged or irritated
by the disc herniation, the patient my
suffer weakness in the Extensor
Hallusis Longus muscle (muscle that
lifts the big toe - classic finding) or the
muscles that dorsi-flex the foot (lift the
foot up) upward. If severe, the patient
will be unable to 'walk on their heals'
with their toes and ball-of-the-foot off
the ground. There is no reliable reflex
test for this nerve root.
L4 RADICULAR PAIN:
If the L3 disc herniates into the 'lateral
recess' (which is where it usually does)
and compresses / irritates the
descending L4 nerve root, the patient
may suffer an L4 radicular pain (aka:
L4 root-pain, or L4 Sciatica). Fig. # 6
shows the regions in the lower limb where the patient will most likely suffer the
symptoms of L4 sciatica (2). As you can see, the majority of patients (75%) suffer
the burning, stinging, and numbing pain of sciatica in the top and inner surface
(dorsum) of the foot, the outer-front of the leg, and the bottom of the big toe.
These pains are the result of damage and irritation to the 'sensory portion'
(portion of the nerve root which connects to skin) of the nerve root.

If the 'motor portion' (portion of the

nerve root which connects to muscle) of
the L4 nerve root is damaged or irritated
by the disc herniation, the patient my
suffer weakness in the quadriceps
muscle (muscle that extend the knee). If
severe, the patient will be unable to
perform a squat or get out of a chair
because. If the problem is severe, the
patient will often have a diminished or
absent Patellar Reflex (aka: knee jerk).

THE CAUSES OF
SCIATICA: [ | Disc
Herniation | The Conundrum |
Discogenic Sciatica | Chemical
Radiculopathy | Autoimmune
Attack | ]
Now that we know what sciatica is, it's
time to try and explain why it occurs--a task easier said than done!
As I see it, there are three possible "causes" of acute sciatica--excluding the
more exotic forms: (1) disc herniation induced sciatica; that is, the
posterior of the disc herniates into the adjacent sciatica nerve root, which in turn
physically compresses and irritates that nerve root into a painful state; (2) grade
V annular tear induced sciatica; that is, the disc rips open and allows
biochemical (cytokines) to leak out and soak the adjacent sciatica nerve root(s),
which in turn inflammes the sciatica nerve root into a painful state; and (3)
discogenic sciatica; that is, the patient may experience a "referred" pain
(that often is dermatomal) down the lower limb from severe irritation of the tiny
sensory nerve fibers (sinuvertebral nerve) that live within the outer 1/3 of the
annulus of the disc. This is NOT an irritation of the actual sciatica nerve but
simply the patient's preception of sciatic nerve irritation--like the left arm pain felt
by someone suffering a heart attack.
In a general sense, disc herniation (25, 70) and/or stenosis are by far the
most frequent causes of compressive sciatica (67-70), there are, however, other
more exotic causes of sciatica; such as, Spondylolisthesis, Piriformis
Syndrome, Obturator Syndrome, Far-Out Syndrome, Synovial Cysts,
Hypertrophied Epidural Vessels, Gas-containing Ganglion cysts, and Tumors.
These rare causes are beyond the scope of this paper.

And before we dig deeping into the phenomenon of sciatica, here is another
important fact that need be remembered: the mechanism of lower limb pain
(sciatica) is most likely VERY complex and is not nearly as simple as the disc
herniates, pinches the nerve, and you get pain. There are many other factors
(some of which that are still unknown) that contribute to the pain of sciatica. In
fact, recently we have learned from the work of Karppinen et al. that neither the
amount of nerve root compression nor the size of the disc displacement
(posterior outpouching of the disc) relates to the amount of pain (VAS) or
disability (Oswestry) the patient suffers (70). Those 'other factors' are still being
debated within the research community, but proinflammatory cytokines
(especially TNF-alpha) are certainly involved (96-99). Pain 'referred' directly from
the disc may also have a role in the sensation of sciatica (11,12).
Let talk a moment about the number one cause of sciatica: The disc herniation.

The Lumbar Disc Herniation:

It has been known for years and is generally accepted that a compressive lumbar
disc herniation is a common cause of sciatica (25,70), and the patients
symptoms will usually depend upon which spinal nerve root is involved. Since
95% of lumbar disc herniations occurs at either the L4 or L5 disc level (290), it's
not at all surprising that sciatica is so very commonly. This high frequency of L4
and L5 disc herniation is also the reason why most EMG-confirmed radiculopathy
occurs in the L5 or S1 root (290).
I'm not going to go into the mechanism of disc herniation on this page since it has
been covered in depth on the 'Disc Herniation Page'. But, figure #3 depicts how
this mechanism works:

Fig. #3 demonstrates a paracentral herniation (pink) of the L5 disc

that is located within a region called the lateral recess. The
herniation is compressing the right S1 nerve root which may cause
'radicular pain' in this patient's S1 dermatome (right lateral foot).
This patient may also have a loss of 'motor function' in the right
lower limb. More explicitly, a loss of muscle strength in
gastrocnemius (calf), and peroneal muscles. There might also be a
lost Achilles' reflex.
THE SCIATICA-HERNIATION CONUNDRUM:
So you think you've got this sciatica thing figured out? It's easy right: the disc
herniates, pinches the sciatica nerve root, and pain occurs in the distribution of
the sciatica nerve. NOT SO FAST!

Although disc hernationinduced sciatica certainly

does occur, it's common
knowledge that not all disc
herniations cause sciatica.
Some people have severe
sciatica without any evidence
of compressive disc
herniation at all!
In a recent investigation by
Karppinen et al. [Karppinen],
it was demonstrated that
20% of severely acute
sciatica patients had no
compressive disc herniation
on MRI; all MRI images were
negative for protrusion,
extrusion, and/or
sequestration, yet these
patients were suffering from
severe back and leg pain!
(70) These researchers
concluded that the severity of sciatica and back pain are NOT
related to the amount of the disc displacement (size of the
herniation) or the amount of spinal nerve root compression!
VAS and Oswestry scores were virtually the same for both disc herniations
patients (disc herniation = protrusion, extrusion, & sequestration) as they were for
disc bulge or normal disc patients! (I would add that patients who were applying
for early retirement were removed from this study which enhances its validity).
(70)
So, if its not a compressive disc herniation that's causing the suffering, then what
it?
One possible explanation was put forth by both Ohnmeiss et al. (619,620) and
Milette et al. (621) These investigators experimentally demonstrated that
disruptions within the substance of the disc (anular tears) not only caused low
back pain but also caused referred pain into the lower limb; we may call this
referred lower limb pain discogenic sciatica. [Ohnmeiss Paper & Milette Paper]
Another explanation is based upon the investigations of Olmarker et al. This
group has repeatedly demonstrated that the application of nucleus pulposus
upon the spinal nerve root can create marked morphological change (axon
damage) and functional change (decreased conduction speed) to the micro-

anatomy of that nerve root, as well as cause pain-related behaviors to occur

within the test animals (790-795).
Therefore, if this nucleus pulposus get loose in the epidural space (most likely
from a grade 5 posterior anular disc tear), it may well cause the pathological
spinal nerve root changes described by Olmarker (790-795) and result in a
painful sciatica syndrome without nerve root compression. Researchers have
termed this phenomenon Chemical Radiculopathy (788,789).
The final theory on non-compression induced sciatica implicates the activation of
the patients own immune system against the nucleus pulposus-soaked nerve
root (800,801). This auto-immune type reaction may help perpetuate the
syndrome of chronic sciatic pain.
Whatever the cause, it is clear that non-compressive disc defects (bulges and
contained herniations) are just as painful and disabling as the classic large
compressive disc herniation. Therefore the symptoms of sciatic patients without
disc herniation in MRI should not be dismissed by the doctor.
DISC HERNIATIONS IN NORMAL ASYMPTOMATIC PEOPLE:
It's common knowledge that not all compressive disc herniations (as seen on
MRI and CT scan) will result in back pain and/or sciatica and are commonly
found in completely asymptomatic people (40-47). I've got a page on the
phenomenon of disc herniations in asymptomatic people ( here: Abnormal MRI in
Pain-Free People ) , but would like to give you all an example and then the
'bottom line' of my research into MRI false positives:

The Bottom-line on the 'False Positives' of MRI:

If I were to gather a group of middle age folks (45 average age) who have
NEVER had back pain before and shoot MRIs on them all, here's what we would
find: 38% would have disc bulges, 37% disc protrusions (aka: contained
herniations), 11% disc extrusions (aka: non-contained herniations), 0% disc
sequestrations (aka: free fragments) and 4% nerve root compression by the disc
herniation. (40-43)
Here's a recap of the main investigations of accuracy of MRI: See the full page
here: (Abnormal MRI in pain-free people)

The below chart shows the percentages of false positive MRI

readings for each type of disc herniations (bulge, protrusion,
or extrusion) and for nerve root compression for a disc
herniation. Remember, none of the below patients had ever

had lower back pain before yet about 3/4 of them had some
type of abnormal disc presentation:
Investigation:

Disc Bulge

Boden et al.
Jensen et al.

Disc Protrusion

Disc Extrusion

20%
52%

Boos et al.

Disc Pathology (Bulge,

Protrusion,extrusion,
sequestration)

Root Deviation or
Compression

NA

27%

1%

80%

63%

13%

76%

4%

Weishaupt et al.

24%

40%

18%

82%

4%

AVERAGES:

38%

37%

11%

79%

4%

And finally, another well known conundrum: the fact that patients radicular
symptoms, clinical neurological presentation, and pain presentation do NOT
always match the level of disc herniation (291)!
So you see, when it comes to diagnosing the cause of disc herniation-associated
sciatica, sometimes things are not always so 'black and white'!

Discogenic Sciatica: Referred pain from the Disc

mimics radicular pain.
Recently, we have learned that the intervertebral disc itself may refer pain down
into the lower limbs in a dermatomal like pain pattern (11, 621). The theory of
Discogenic Sciatica is complex and still controversial but can be explained as
follows: just as a person who is having a heart attack will often suffer a 'referred
pain' down the left arm, a person with massive pain generation within a disrupted
and/or diseased lumbar disc may also suffer a referred pain down into the leg,
often in a dermatomal-like pain pattern. Ohnmeiss et al. has extensively
investigated this theory and has done a good job at proving its existence (11).
This phenomenon can make it very difficult to ascertain just exactly what is
causing a patients sciatica: Is it from a disc herniation compressing the adjacent
nerve-root, or from a severely internally disrupted disc referring pain, or a
combination of both? This referred pain from the disc into the lower back and/or
lower limbs is called Discogenic Pain or as I like to call it, Discogenic
Sciatica.
Milette et al. has also investigated the phenomenon of discogenic referred pain
and demonstrated that disruptions within the disc can indeed refer pain into the
back and down the leg. Read the full paper here: (Milette - 1995: Discogenic
Sciatica)

I will be devoting an entire page to this theory in the near future and will be
presenting some real cases of 'Discogenic Sciatica' from an upcoming
investigation that I will be writing with Dr. Jinfu Lin of Taiwan China.

Chemical Radiculopathy: A leaking disc may

result in radicular pain.
Another possible cause of sciatica is called Chemical Radiculopathy
(257,258). This is believed to occur when the disc rips open and leaks without
disc bulge or herniation. It has been proposed that certain biochemicals
(especially proinflammatory cytokines) may leak from a completely disrupted
disc (a disc with a hole in it), soak the adjacent nerve root and cause a
'Biochemical irritation' to that nerve root, hence inducing radicular
pain(153,155.550). Again we have a situation where radicular pain may occur
without the presence of a disc herniation!
Although this theory is relatively new, I'm convinced that it happens all the time.
Not only have I seen this time and time again in my own clinical practice, I've just
recently seen it occur in two of our local medical doctors who I personally know
(one's a neurosurgeon and the other's a neurologist). Both had come down with
real root-related sciatica (confirmed by EMG) despite having a completely normal
looking MRI!
Numerous animal investigations has confirmed that the presence of nucleus
pulposus on spine nerve roots is a 'bad thing'(551,553-558,560)! Nucleus
pulposus and the biochemical Tumor Necrosis Factor - alpha have been linked to
some truly damaging effects on spinal nerve-roots, such as: Wallerian
degeneration of the axons within the nerve root; a characteristic myelin injury to
the axon (551,553-555); a local increase in vascular permeability with the nerve
root (556,557); intravascular coagulation within the nerve root (551,558); reduced
intraneural blood flow within the nerve root(560); leukotaxis (558); macrophage
recruitment within the nerve root; and a splitting of the myelin sheath from the
axon (140, 141).

AUTOIMMUNE ATTACK:
The final theory on non-compression induced sciatica implicates the activation of
the patients own immune system against the nucleus pulposus-soaked nerve
root (800,801). This auto-immune type reaction may help perpetuate the
syndrome of chronic sciatic pain. Again, this is a very complex subject, and I will
be devoting an entire page to it in the near future.

RISK FACTORS FOR THE DEVELOPMENT OF

SCIATICA:

Beside having bad genetics for disc building material, which is probably the
number-one risk factor for disc herniation-associated sciatica, the line of work
that you choose may significantly increase or decrease your livelihood of
developing disc herniation-associated sciatica. Research has indicated that
'heavy manual labor' and 'sedimentary work' are the two types of employment
most frequently associated with the development of sciatica (195). More
explicitly, investigations have demonstrated that frequent heavy lifting, (193,194)
frequent twisting and bending, (193,194) exposure to vibration,(192,193) and
sedentary activity (192,195) [190] all increase the risk of developing sciatica.
It seems the 'safest' type of work (the work in which less people develop sciatica)
is that which combines a combination of sitting standing and physical activity
(195).

A CURE FOR SCIATICA? INFLIXIMAB &

ETANERCEPT (False hope: 2005 update )
It is currently believed by some investigators that the cytokine 'Tumor
Necrosis Factor - alpha' (TNF-a) is one of the "smoking guns" of sciatica as
it has been shown to be directly involved in nucleus pulposus-induced nerve root
damage (4). It has been experimentally demonstrated in both the animal and
human that the chimeric antibody 'Infliximab' stops and minimizes nerve root
damage after the application of nucleus pulposus upon a nerve root (animal
studies) and significantly decreases the lower limb pain in acute sciatica sufferers
(140). Although the use for Infliximab looks promising to combat sciatica, a larger
randomized study is desperately needed to confirm the results of Karppinen's
initial pilot study of 2003 (140) and recent 2005 one year follow-up on these 10
patients (900).
Although Infliximab has already been proven safe and effective for the treatment
of other diseases of the body, such as rheumatoid arthritis (144,145), plaque-type
psoriasis (146), active ankylosing spondylitis (147), and Crohns disease (148),
further investigation is needed before sciatica can be added to the list of
indications for the drug Infliximab (140).
UPDATE (2005) Unfortunately, It would now appear that Infliximab is no
more effective than placebo for the treatment of disc herniation related
sciatica. In a larger randomized controlled investigation, Karppinen et al.
discovered that patients given placebo (fake) injections obtained just as much
sciatic pain releif as those who got the injection of the "ultra-expensive"
infliximab:

Korhonen T, Karppinen J, et al. "The treatment of disc herniation-induced

sciatica with infliximab: results of a randomized, controlled, 3-month follow-up
study." Spine 2005 Dec 15;30(24):2724-8.
Department of Physical Medicine and Rehabilitation, Oulu University
Hospital, Oulu, Finland.
STUDY DESIGN: A randomized controlled trial. OBJECTIVES: To evaluate
the efficacy of infliximab, a monoclonal antibody against tumor necrosis factor
(TNF)-alpha in a randomized controlled setting. SUMMARY OF
BACKGROUND DATA: Recently, we obtained encouraging results in an
open-label study of infliximab in patients with disc herniation-induced sciatica.
Furthermore, the results of experimental studies support the use of infliximab
in sciatica. Therefore, we initiated a randomized, controlled trial (FIRST II,
Finnish Infliximab Related STudy) to confirm the efficacy of a single infusion
of infliximab for sciatic pain. METHODS: Inclusion criteria were unilateral
moderate to severe sciatic pain with an MRI-confirmed disc herniation
concordant with the symptoms and signs of radicular pain. Patients had to be
candidates for discectomy, as evaluated by an independent orthopedic
surgeon. Forty patients were allocated to a single intravenous infusion of
either infliximab 5 mg/kg or placebo. Assessments at baseline and various
time points included clinical examination with measurement of straight leg
raising restriction; questionnaires related to subjective symptoms (leg and
back pain by 100-mm visual analog scale, Oswestry disability); sick leaves;
number of discectomies; and adverse effects possibly related to treatment.
The primary endpoint was a reduction in leg pain from baseline to 12 weeks,
which was analyzed using a Mann-Whitney U test and repeated-measures
analysis. RESULTS: A significant reduction in leg pain was observed in
both groups, with no significant difference between treatment regimens.
Similar efficacy was observed between treatment groups for secondary
endpoints. Seven patients in each group required surgery. No adverse effects
related to treatment were encountered. CONCLUSIONS: The results of this
randomized trial do not support the use of infliximab for lumbar
radicular pain in patients with disc herniation-induced sciatica.

UPDATE 2007:
Now, Etanercept, another TNF-a inhibitor (a fusion protein) has been shot
down by a grade "A" randomized placebo-controlled double blind trial. In 2007,
John Hopkins School of Medicine's SP Cohen, et al published the results of their
investigation into the off-lable use of Etanercept for the treatment of sciatica.
Unfortunately, they discovered that this very expensive treatment is no better
than that of a placebo (suger pill). They concluded, "A single low dose of

intradiscal etanercept does not seem to be an effective treatment for

chronic radicular or discogenic low back pain."

TREATMENT OPTIONS: [Surgery Timing | Surgery

Indications | Treatment Guidelines ]
Warning: These recommendations are for educational purposes ONLY and
should never be substituted nor could nerve take the place of an examination
by your medical doctor! Do NOT implement any of these courses of treatment
without the approval of your medical doctor.
Without question, the best treatment for non-complicated sciatica is passage of
TIME. Even the worst cases of sciatica may spontaneously resolve with time,
and even some very large disc extrusions may completely be reabsorbed by the
body (23), hence decompressing the nerve root naturally. BUT, if you are a
candidate for surgery and are not improving with care at all, then delaying the
surgery seems to decrease your chances for a successful surgical out come
(305).

FOUR INDICATIONS FOR SURGERY:

The American Academy of Orthopedic Surgeons and Alf
Nachemson who is the number one spine researcher in the world - (18)
recommends the following conditions be met before decompressive surgery is
offered:

#1

Functional incapacitating pain in the leg, extending below the knee with a nerve root distribution.

#2

Nerve root tension signs (positive straight leg raising test) with or without neurologic
abnormalities, fitting the radiculopathy.

#3

Failure of clinical improvement after 4-8 weeks of conservative treatment,

#4

Confirming imaging study: abnormal myelogram, computed tomogram (CT), or magnetic

resonance imaging (MRI) correlated to the physical signs and distribution of the pain.
The only ABSOLUTE indication for surgical intervention, however, is if the patient
develops a loss of bowl or bladder control (cauda equina syndrome); if the
patient develops severe progressive motor loss in the lower limbs, such as footdrop; or if the patients has severe debilitating pain.
Several high quality outcome assessment investigations have shown that even
patients with confirmed radiculopathy (nerve root damage) that meet the 'four

criteria' for surgery often do 'well' with non-surgical treatment (77 - Saal & Saal);
furthermore, although patients who undergo discectomy seem to get better faster
(rarely 100% better), in the long-run (4 to 7 years) the non-surgical patients
obtain nearly the same improvement in terms of pain relief and functional
outcome. (78 - Weber)

SURGERY TIMING: When to "Pull the Trigger" and

Try Surgery?
It is generally agreed upon, assuming the patient is NOT improving, that one
should not wait too long before undergoing decompression via discectomy. The
the experts can't seem to agree upon is how long the patient should be allowed
to suffer. The forthcoming investigations all yield different opinions on when
surgery should be performed; however, they all agree that a suffering patient
should not wait longer than one year. The average time is currently 4.6 months,
so waiting longer than this might decrease your chances of having a successful
discectomy. I would seem to be living proof of this, i.e., I waited 15 months and
my surgery failed miserably.

Research papers:

Year (foot note)

Length of conservative care:

Postacchini F.

1999 (14)

6 months

Dvorak J, et al.

1988 (11)

4 months

Hurme M. & Alaranta H.

1987 (12)

2 months

Rothoerl RD , et al.

2002 (26)

2 months

Ng LC & Sell P

2004 (66)

< 12 months

Dauch WA , et al.

1994 (10)

6 weeks

Average suffering periods for all

investigations: After this time, your
chances of discectomy success may
drop.

4.6 months

Treatment Guide-lines:
Ive read a tremendous amount of research and picked-the-brain of many a
doctor during my own battle with sciatica. Based on my research and personal
experience I've developed some recommendations for the treatment of sciatica:

Start anti-inflammatory medication such as Naproxen, Ibuprofen, and

Celebrex, as soon as possible. The sciatic-inflamation associating is
becoming stronger and stronger, so anti-inflammatory measures are a
must.
Take aspirin per day to thin the blood. This may help prevent
clotting and venous stasis within the of microvasculatory system
within the delicate nerve root. It is believed that damage to this microcirculatory system within the delicate nerve may lead to permanently
axon death, scaring within the nerve root, chronic hypersensitivity of
the nerve root and chronic pain. (Remember to check with your MD first!)
Get at least one transforaminal epidural steroid injection (aka: TFESI)
performed under done under fluoroscopy at all suspected root
levels. Don't monkey around with nerve root blocks UNLESS they
administer the steroid immediately afterwards.
Start conservative care promptly:this may include physical therapy,
exercise, swimming, traction and/or Chiropractic care. Try and stay as
active as possible without aggravating your pain. Home traction
devices and/or a slant board are also worth trying.
Try a 14 day course of oral steroids (prednisone) to help reduce
inflammation that might be occurring in an area that was not reached
by the epidural injections.
At the three-month-mark, if youre NOT IMPROVING, get an
immediate neurosurgical opinion! You absolutely do NOT want to

wait too long for an indicated surgery. Numerous research papers

have found that your chances for a successful surgery decrease with
the passage of time after the 3 or 4 month mark (301-309).

WHAT ARE MY CHANCES OF GETTING

SCIATICA?
For the answer to this question, we must turn the giant population based survey
studies which are mostly flawed with respect to sciatica, for they dont
differentiate between true root related sciatica, and fake sciatica (referred lower
limb pains from the SI joint, intraspinal ligaments, and/or facet joints etc).
From these less specific studies we have learned that the life-time chance
(prevalence) for developing generic sciatica (sciatica of unknown cause) is
about 35%; this number has been pretty well substantiated in other investigations
as well (181,183-186). Over the course of each year, about 1% of the North
American population will suffer an attack of sciatica (9); that equates to about 4.9
MILLION cases per year!
Only two groups of investigators has had the intelligence to address the life-time
prevalence of true root-related sciatica: Heliovaara et al. found that 5% of men
and 4% of women will develop nerve root-related sciatica at some point in there
life (181). These numbers were later confirmed by Manninen P, et al in 1995
(182).
The differentiation between the life-time chances of generic sciatica (35%) and
true root-related sciatica (5%) demonstrates that true root-based sciatica is a
relatively rare phenomenon. (Dont we feel special?)
There are no studies that have investigated the prevalence for discogenic
pain/sciatica in the population, but Im guessing it to be around 1% or 2%.

WILL I RECOVER FROM SCIATICA? [ Pertinent

Research outcome ]
The short answer: probably not 100% if your sciatica is a true radiculopathy
confirmed by EMG and/ or severe.
Unlike lower back pain, sciatica has a more prolonged and less certain recovery
period. For the general non-radiculopathic sciatica, 40% to 50% of those affected
will completely recovery within 4 weeks (19,20), and 88% will recovery within 6

months (8); however, 5% to 10% will not recover and require surgical
decompression (9).
For us patients with 'real' disc herniation-associated radicular pain
(radiculopathy), the outcome is less favorable, as has been demonstrated by
several well-written investigations: Only 37% will completely recovery
from there radicular pain (sciatica) by 3.5 years! This number was
derived by averaging out all the complete recovery patient from the major five
outcome studies of our time. (here)

The Outcome Studies:

The Saal Study:
The Saal brothers 1989 outcome study is undoubtedly the best paper to date on
the recovery-rates for radiculopathy-related sciatica: the Saals followed 58
patients who had confirmed disc herniation-induced radiculopathy (via MRI &
EMG). They had all failed passive conservative care and were put through the
authors aggressive conservative care program, which included special exercises,
medications, epidural steroid injection and physical therapy. After 2 years,
only 30% of the patients reported a full recovery and 10% were lost to
surgery. The good news - if youre not an athlete - is that 90% of the patients
returned to their original work and recovered enough to at least be able to
perform some limited recreational activities (77).
The Atlas Study:
Atlas et al. followed 220 patients that were treated surgically for disc herniationinduced sciatica and 183 patients who were non-surgically treated for the same.
At five years only 28% of the surgically treated patients reported that their pains
were completely gone. The conservatively treated group faired even worse, in
that only 12% reported a complete resolution of their symptoms (15).
The Nykvist Study:
Another outcome study by Nykvist et al. found that after five years of either
surgical or non-surgical treatment; 82% of the non-surgically treated group and
62% of the surgically treated group still suffered with at least some degree of
sciatica (17)!
The Weber Study #1:
Weber et al. studied the outcome for a group of 208 non-surgically treated
patients, all of whom had root symptoms associated with sciatica. After one

year, 30% of the patients had reduced capacity in work, and restrictions of leisure
activity and only 50% reported no pain at work or leisure (19).
The Volvo Award Winning Weber Study:
In the only quality randomized outcome study to date, Henrik Weber followed a
group of 126 sciatica patients who were randomly assigned to either surgery or
non-surgical care. All of these patients were considered boarder-line surgical
candidates and were followed for over 10 years. Over that 10 year period, only
5% of the patients were lose, which gives this Volvo Award Winning study
excellent predictive value. At four years post treatment, only 66% of the surgical
patients were completely satisfied with their outcomes, versus only 52% of the
conservatively treated group. At 10 years, only 58% of the surgical group were
completely satisfied (some had worsened), and 56% of the conservative group
were completely satisfied. At 10 years only 2% of both groups reported residual
lower limb pains (sciatica), which was greatly improved from the 37% and 23%
residual sciatica reported sciatica at 4 years (16).
The Balague Study of 1999: (126) This group of Swiss and American
investigators study the outcomes of 82 'severe sciatica patients' - patients were
hospitalized because of the severity of their sciatica. 33% of the patients were
lost during the one year follow-up period to surgery, although they were still
followed up. As for the recovery of this cohort, the authors stated the following,
"...a substantial percentage of patients with acute severe sciatica had not
recovered by 1 year after discharge." More explicitly, only 21 (29%) of the all 82
patients were "essentially" pain free at one year. Interestingly, only 74% of these
patients had disc herniation on MRI, and only 62% had a positive EMG!

The Bottom Line:

Radiculopathy Outcome Studies:

Complete Recovery or
Completely Satisfied with
Outcome:

Saal & Saal. 1989 (77)

30% (conservative) @ 2 years

Atlas et al. 2001 (15)

28% (surgical) 12% (conservative) @ 5 years

Nykvist et al. 1989 (17)

38% (surgical) 18% (conservative) @ 5 years

Weber et al. 1993 (19)

54% (conservative) @ 1 year

Weber. 1983 volvo award (16)

66% (surgical) 52% (conservative) @ 4 years

Balague et al. 1999 (126)

29% (surgical & conservative) @ 1 year.

Average % of Complete Recovery: (I took the

average from all 6 investigations, also

ONLY 37% of sciatica patients,

with or without surgery, recover

averaged surgical & conservative, when

completely or near completely (33%
applicable, into one number before computing from conservative care and 40% from
final number.)
surgical care).
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GENERAL INFORMATION:
The term "Spondylolisthesis" refers to a condition where one of the vertebrae
(usually L5) becomes misaligned anteriorly (slips forward) in relation to the
vertebra below. This forward slippage - as noted in fig. #1 - is caused by a
problem or defect within the pars interarticularis (aka: pars, red arrows fig.
#1). Occasionally, facet joint and/or posterior neural arch defects may also cause
this syndrome as well. The forward slippage does NOT always occur; however,
the par defect, which is considered a non-united childhood fracture by some
(134), still may be present. This non-slipped pars defect is called a
"Spondylolysis" and is almost always a precursor to the actual forward
slippage.

The

aforementioned structures (pars interarticularis, facets, neural arch) are

responsible for holding the anterior portion of the vertebrae (vertebral body) in
perfect alignment. Maintaining this alignment is critical in order to keep the spinal
exit-holes, (aka: neuroforamen), which are where the delicate spinal nerves exit
the spine, large and open. Any narrowing of the neuroforamen may result in
compression of the ultra-sensitive exiting spinal nerve root and dorsal root
ganglia that in turn may well result in back pain.
The pars interarticularis, as noted above in Fig. #1, is the weakest and thinnest
region of the lumbar vertebra. In some unlucky individuals, the pars may only be

able to tolerate the 'activities of daily living' (135) and is easily fracturable with
repeated loadedflexion (136) and
axial rotation. (139)
Figure #6
demonstrates an
isthmic grade 2
spondylolytic
spondylolisthesis with
a severe loss of disc
height in a 28 year
old patient with low
back pain and some
radiating lower limb
pain that traveled to
the knees. As you
can see, there is a
very visible pars
defect (green arrow)
that has allowed the
L5 vertebra to
translate (slid)
forward by about
50%.
Flexion/Extension
films revealed that
this condition was
stable and he
responded nicely to
flexion/distraction,
activator, and exercise.

Grading the Spondylolisthesis: (Fig.#6)

Spondylolisthesis may be classified/graded by noting the degree of anterior
translation (forward slippage) of the top vertebral body in relationship to the
bottom vertebral body: Slippage from 0-25% is called a Grade I
spondylolisthesis; from 26-50% is called a Grade II; from 51-75% is called a
Grade III; from 76-100% is called a Grade IV; and anything greater than
100% is called a Grade V spondylolisthesis.
It is generally agreed that inheritance plays a "major role" in the development
of a pars interarticularis defect, for the prevalence of spondylo is much greater

within a family-tree than in that of the general public. (8,240-242, 244) Wiltse has
proposed that a hereditary defect or dysplasia in the cartilaginous model of the
posterior neural arch is what predisposes folks to spondylo. (245)
Professor Nikolai Bogduk, who is the number 1 functional anatomist in the world
and a two time Volvo Award Winner, has the following opinion on the origin of
spondylolysis: "The biomechanical and epidemiological evidence points to pars
defects being an acquired fracture, either as a result of single, severe trauma or
as a result of fatigue failure." (136,138,150,152,153)[126]

Occurrence Rate and Natural History: The

Fredrickson Study:
In 1984 Fredrickson published a fascinating investigation into the natural history
of spondylolisthesis/spondylolysis (spondylo) that demonstrated the majority of
spondylos asymptomatically occur by age 12 and only become symptomatic in
only 13% of the cases. Rarely (3%) will the pars defect ever completely heal.
Males are affected twice as frequently as females. (8)
More explicitly, Fredrickson x-rayed 500 asymptomatic six year-olds and then
followed the kids for over 20 years! Amazingly, all of the kids who were
diagnosed with spondylolysis or spondylolisthesis completed the 20 year study
and were not lost! The entire group of kids were re-X-rayed every 4-5 years and,
if pain had developed, re-examined. At age six, 4.4% of the kids had either
isthmic spondylolisthesis or spondylolysis on x-ray. By age twelve, 5.2% had the
defect (85% participation rate). This increased to 6% by age eighteen; however,
the majority of the non-spondylo kids had dropped out of the study by this time
(34% participation rate). From the aforementioned percentages, it can be
calculated that about 66% of all spondylolistheses/spondylolyses occur by age
twelve and are asymptomatic in the overwhelming majority of the cases. (8,502)
Back pain developed by age 14, 16, 22, and 27 in only four of the participants
and one surgery was necessary to correct a disc herniation that developed above
the spondylolisthesis. Only 1 of the 30 spondylolyses completely healed,
although this healing didn't occur until the kid was in her late twenties!
Fredrickson also reviewed the spine x-rays of 500 newborns and could not find
one single case of spondylolysis or spondylolisthesis; this finding had been
previously verified by many other investigations. (204,208,211,224) In 10 of the
kids, a spondylolysis developed between the x-ray intervals; none of these new
pars defects were painful as the kids and their parents reported no back pain had
occurred during that interval. In 7 of the 30 patients with spondylo, a progression
of the slippage or initial slip occurred by age 16; again, the slippage
appearance/increase was not associated with pain. The authors concluded that
the "development of the pars interarticularis defect, with or
without spondylolisthesis, does not cause pain in most patients."
(8)

In spondylolisthesis or spondylolysis, a "fibrous tissue" will form within the crack

(defect) within the pars. (131) This "fibrous tissue" contains nerve fiber and paincarrying free nerve endings (133) that contain neuropeptides (134); therefore,
this tissue is theoretically capable of transmitting PAIN-signals to the brain [in
layman's terms: this scar tissue like stuff that fills the crack in the back bone, has
the potential to cause back pain.]
Fig. #2 represents a grade II Isthmic spondylolisthesis, which is the most
common form of spondylolisthesis in people under 50 years of age (40). About
90% of these spondylolisthesis' occur at the L5 vertebral level (37). The
prevalence rate (rate naturally occurring in a given population) of spondylolysis in
the general population is about 7%
(502); however, in Alaskan Eskimos the
prevalence rate is between 28% (11)
and 40%! (10)
In Fig. #2 you can see that a "crack" or
"pars defect" that has occurred within
the pars interarticularis of the L5 neural
arch. Because of the defect, the L5
vertebral body has slid forward by over
25% as measured against the sacral
base below; anterior translation has
occurred. This condition is called a
"spondylolytic spondylolisthesis."
Also notice that the thecal sac (yellow)
has been kinked by the forward
translation. the nerve roots (not shown)
are undoubtedly compressed. If
severely symptomatic, a surgical
procedure called a Fusion (LAIF or
PLIF) may be indicated to realign the
vertebrae and restore the lateral and
central canals to their original size that
accommodates the adjacent neural
structures.
In real life, the large and jagged "pars
defect" is filled with a fibrous tissue that
is, unfortunately, filled with nerve fiber
that has the ability to carry pain signals
to the brain. (133,134)

Spondylolistheses are categorized or graded on the degree of forward slippage

that has occurred. The bone/sacrum below is divided into four equal sections as
noted in Figure # 3.
Figure #3 demonstrates a Grade II spondylolytic spondylolisthesis. Note that the
L5 vertebra has translated (slipped
forward) by over 25%. This 35%
slippage is categorized as a grade II
spondylolisthesis.
Also note the fibrotic tissue (green)
that fills in the pars defect.

THE RESEARCH:
DOES SPONDYLOLYSIS
AND/OR
SPONDYLOLISTHESIS
CAUSE PAIN. [ Torgerson et al. |
Fredrickson ]
In 2003, Beutler and Fredrickson
published the continued results of the
ONLY prospective investigation into
the natural history of
spondylolisthesis / spondylolysis
(spondylo) after monitoring 30
afflicted volunteers for more than 45
years! After the last of many follow-up
evaluations (which included MRI, Xray, and SF-36), the researchers
concluded that spondylo is not
associated with future chronic pain,
impairment or disability. More explicitly,
at the 45 year mark, all categories of
the volunteers completed SF-36 testing (the number one physical and mental
health assessment form) was nearly identical to that of a normal population for
the same age group. In other words, the spondylo people had the same quality of
life as the rest of the population for that age group. These findings lead the
authors concluded that the current study demonstrated that a unilateral pars
defect is not associated with further slip or disability, and subjects with a
bilateral pars defect follow a clinical course similar to that of the general
population.
OTHER INVESTIGATIONS:

Furthermore, it is common knowledge that spondylolysis and spondylolisthesis

are seen with equal frequency in both asymptomatic people and symptomatic
people (501,512), and the degree of forward slippage is in no way correlated with
the degree of patient pain or disability. (16,46)
More explicitly, in 1982 Libson and Dinari radiographically studied the occurrence
rate (prevalence) of spondylolysis / spondylolisthesis in 936 asymptomatic (pain
free) and 662 symptomatic (back pain suffering) military soldiers concurrently.
They discovered that just as many pain-free soldiers had spondylolysis and/or
spondylolisthesis on X-ray as did the soldiers who had symptomatic back pain,
i.e., 10% of the asymptomatic soldiers and 9% of the symptomatic soldiers had
spondylolysis/spondylolisthesis on radiograph. (501)
However, in 1976, Torgerson et al. concluded, "Our findings indicate that this
lesion [spondylolisthesis and spondylolysis] is often symptomatic.... Statistical
interpretation indicated a significantly greater correlation between symptoms and
the existence of spondylolysis and spondylolisthesis (p > 0.005). " The only
problem with this investigation, which used x-ray to assess listhesis (forward
slippage) and/or pars defect, was the fact that no oblique radiographs were made
of the lumbar spine; therefore, this made iit extrememly difficult to assess the
pars. This was probably the reason that the prevalance rate (4.7% and 1.4%)
was so low in both groups.
Other investigators have confirmed the prevalence rates in the aforementioned
findings in pain-free people:
Recently, in 2005 Beck et al. published the results of a very large investigation
into the prevalence of spinal anomalies in patients with back pain. After studying
the radiographs of 1004 patients presenting to a New Zealand chiropractic clinic
for back pain, 7.8% had spondylolisthesis. (502)
In 1966 a famous and often quoted investigation by Moreton investigated the
prevalence (occurrence rate) of spondylolysis within 32,600 asymptomatic
people who were X-rayed as part of a pre-employment screening. The
prevalence of spondylolysis in this group of 18 to 35 year olds was 7.2%. (503)
Other investigation have concluded this same prevalence rate. (8,512)
The aforementioned investigation (512), prompted Professor Nikolai Bogduk,
MD, researcher, author, and two-time Volvo Award winner to proclaim within the
Australasian Faculty of Musculoskeletal Medicine Guidelines that finding a pars
defect on a plain film does not constitute establishing a diagnosis of the patient's
pain. (500) Two other research giants, Schmorl and Junghans, have also
proclaimed that pain specifically related to spondylolysis and/or spondylolisthesis
does not exist. (27)

However, in either spondylolisthesis or spondylolysis, the fibrous-filled defect that

forms within the pars (131) certainly has the potential to generate back pain, for it
contains both nerve fiber and pain-carrying free-nerve endings (133) that contain
neuropeptides (134).

CLASSIFICATION OF SPONDYLOLISTHESIS:
The most widely used classification system was developed by Wiltse et al. back
in 1976 (36) This system described five distinct types of spondylolisthesis:
1.) Dysplastic Spondylolisthesis: Congenital malformation of the sacrum or
neural arch of L5.
2.) Isthmic Spondylolisthesis: Stress fracture, elongation, or acute fracture of
the pars.
3.) Degenerative Spondylolisthesis: Long-standing arthritic process of the
zygapophyseal joints.
4.) Traumatic Spondylolisthesis: Neural arch fracture excluding the pars
region.
5.) Pathologic Spondylolisthesis: Bone disease - Paget's, Metastatic disease,
or Osteopetrosis.
6.) Iatrogenic Spondylolisthesis: Man-made following lumbar spine surgery via
LAIF or Laminectomy.
Now, let us look at the more common forms of spondylolisthesis:
DYSPLASTIC SPONDYLOLISTHESIS: (aka: Congenital Spondylolisthesis)
This type of spondylolisthesis results from a congenital (from birth) malformation
(aka: dysplasia or defective growth/development) of the neural arch of the
vertebra and/or upper portion of the sacrum. More explicitly, the articular
processes of the vertebrae are tipped too far forward, the facet joints are facing
forward (sagittal or axial) instead of sideways (coronal), and/or there is a
malformed sacrum with spina bifida that allows spondylolisthesis.
Although fairly rare, 14-21% of all discovered spondylolisthesis are the result of
the the aforementioned congenital malformations. (1) Isthmic spondylolisthesis,
however, is four times more common. (40) When dysplastic spondylolisthesis
occurs, it's usually quite severe. (40)
Unlike the other forms of spondylolisthesis, the dysplastic variety has a possible
genetic predisposition. More explicitly, Wynne-Davies et al. (2) X-rayed 147 first-

degree relatives of patients with spondylolisthesis. The results indicated that 33%
of the relatives also, unknowingly, had dysplastic spondylolisthesis. This is fourtime higher than what would be expected in the normal population where 8% is
the population prevalence for spondylolisthesis. (500,501,502,512) Other
investigators have also reported a familial predisposition as well (3).
ISTHMIC SPONDYLOLISTHESIS: (aka: Lytic Spondylolisthesis)
In people under the age of 50, Isthmic spondylolisthesis is the number one type
of spondylolisthesis encountered and has not been noted in infants (40). The
reported prevalence rate (how frequently seen) in the US population is between
6% and 7% (5), although its X-ray presents is certainly not always associated
with back pain.
(500,501,502,512) There are
three "sub-types" within this
category:
SUB-TYPE A: (aka: Lytic
Spondylolisthesis)
Sub-Type A is the most
commonly found type of
spondylolisthesis in people
under 50 years of age (40). It
is believed that
"biomechanical stress," such
as repetitive mechanical
strain from heavy work or
sports, causes a fatigue
fracture within the pars
interarticularis (26) that in
turns allows the defective
vertebra to move forward in
relationship to the sacrum or
vertebra below.
Figure #7 denotes such a
condition: Yellow arrows point
to a marked radiolucency
(black area) through the pars
interarticularis, which is highly
indicative of a bilateral par
fracture. The L5 vertebra has
slide about 20% forward as
indicated by the Red Arrow;

therefore, this would be called a Grade 1 Isthmic Spondylolisthesis - Sub-type

A.
Interestingly, there does seem to be a familial predisposition for Isthmic
spondylolisthesis, for 15% of first-degree relatives of people with Isthmic
spondylolisthesis will also have spondylolisthesis (2); this 15% prevalence is
double the natural occurrence rate of spondylolisthesis of 6-7%. (501,502,512)
In a recent clinical guideline, Dr. Nikolai Bogduk MD, PhD, author, and Volvo
Award Winner, stated, The biomechanical and epidemiological evidence points
to pars defects being an acquired fracture, either as a result of single severe
trauma or as a result of fatigue failure (19,21,32,34,35). (500) The fibrous
tissue that fills the defect may contain osseous debris that is evidence of its
traumatic origin (17).
SUB-TYPE B:
This type of Isthmic spondylolisthesis is characterized by a elongated pars
without separation. It is believed that the elongation occurs secondary to
"repeated, minor trabecular stress fractures of the pars." (26) Each time these
possible sub-acute stress fractures occur and heal, the vertebral body is
displaced farther and farther forward. Eventually, the pars may fail to heal and
result as a full pars defect; therefore, it may be impossible to differentiate
between Sub-Type A and Sub-Type B categories.
SUB-TYPE C:
These types of spondylolisthesis' are extremely rare and result from an acute
pars fracture, often as result of traumatic lumbar hyperextension injury;
displacement seldom occurs. (39)
DEGENERATIVE SPONDYLOLISTHESIS: (aka: Pseudospondylolisthesis,
nonspondylolytic spondylolisthesis)
This is the most common form of spondylolisthesis in patients over 50 years of
age and rarely occurs in those under 50. There is no fracture or elongation of the
pars interarticularis and the neural arch is intact. The mechanisms of forward
displacement are thought to involve a combination of "zygapophyseal joint
arthrosis, disc degeneration, and remodeling of the articular processes and pars."
(26,41) On X-ray, a widened "Pedicle-facet angle" is one of the tell-tale signs of
degenerative spondylolisthesis. Finally, so some strange reason, Degenerative
Spondylolisthesis has an affinity for affecting Females, at L4, who are over 40.
[The 3 F's of degenerative spondylolisthesis.]
TRAUMATIC SPONDYLOLISTHESIS:

This type of spondylolisthesis, which is extremely rare, results from a

traumatically-induced fracture to the neural arch other than the pars region. The
"Hangman's Fracture" in the cervical spine's second vertebra (Axis) is a common
and often deadly example of such a traumatically induced phenomenon. This
type of fracture is extremely rare in the lumbar spine.
PATHOLOGICAL SPONDYLOLISTHESIS:
Generalized or systemic disorders of bone may affect the neural arch of the
spine and allow spondylolysis or spondylolisthesis to occur. Metastatic carcinoma
(cancer), osteopetrosis, and Paget's disease are some of the more common
disorders that may contribute to the formation of spondylolysis. (26)
IATROGENIC SPONDYLOLISTHESIS:
Iatrogenic (man-made) spondylolisthesis is a complication of lumbar anterior
interbody fusion (LAIF), which ironically is often used to stabilize
spondylolisthesis. Either the vertebrae above of below develops a pars fracture
and possibly forward slippage from the extra stress placed upon that segment
from the surgery. Laminectomy procedures, which are used for decompressing
symptomatic disc herniations in the spine, will result in an overload of weightbearing stress on the contralateral pars and, in some patients, result in a pars
fracture.
DIAGNOSTIC TECHNIQUES:
In 1994 Suh et al. described a technique for differentiating between a
symptomatic pars defect and non-symptomatic pars defect. They simply
anesthetized the suspect with lidocaine to see if this affected the patients pain. If
so, then the pars was named a pain-generator and surgery proceeded. (154)
Bogduk also described this 'pars block' in his recent book entitled "Medical
Management of Acute and Chronic Low Back Pain." More explicitly, Bogduk
stated the following: "The definitive test of whether a pars defect is symptomatic
is to anaesthetise the [pars] defect. (154) Pars blocks are the only means
available by which to determine whether or not a radiographically evident defect
is a symptomatic or an asymptomatic one. Such a test is imperative in view of
the high prevalence of defects in asymptomatic individuals." (126)

QUIZ:

What you all you

experts think of this,
Figure #8:
This is a grade 3
spondylolytic
spondylolisthesis.
Note the forward
slippage of L5 upon
the sacrum that is
slightly greater than
50%. There is a huge
pars defect as well.
Can't see it? Go here.
I have drawn in some
lines that should help
you see it.
Also note that the L5
disc is almost
completely gone
(discopathy). It's
almost bone on bone
between L5 and the
sacral base.

|||| Level One Exercises |||| Level Two Exercises |||| Doug's Core
Program ||||

ALWAYS START YOU WORK-OUT WITH THIS

STRETCH. Simply get in the above position and
GENTLY pull your knee to your chest and hold for a
count of 20 to 30 seconds. Slowly lower the leg
and repeat the other side. Do each leg 3 times. Do
NOT force it or cause yourself any significant lower
back pain. It's also easy to stretch the Piriformis
Muscle in the 'up' position (grey leg). All you do is
move your left heal toward the right knee (rotates
the knee and hip) while you keep your knee in about
the same place. DO NOT do this (piri stretch) if you
have bad knees!

Assume the above position only put the grey arm

straight over-head and the white arm down by your
side. Now, tighten your tummy (and butt if your not
too sore) to lock your spine in place. Slowly lift the
grey arm upward like a railroad crossing-gate; keep
it moving until it rests on the ground next to your
side. SIMULTANEOUSLY do the same thing with
white arm (right) ONLY IN THE OPPOSITE
DIRECTION. Both arms are going in opposite

Since disc patients lose their ability to

'Reflex-Contract' their core spinalstabilizers, learning how to 'manually'
accomplish this is a must! Here's how:
Simply suck / contract your belly-button
downward (NOT by deeply inhaling!) and
tighten your buttock muscles and your
anus muscle (as in trying desperately to
hold in a threatening fart!)
SIMULTANEOUSLY and HOLD. IF you're
really in pain (acute) DO NOT DO THE
BUTT AND ANUS MUSCLE PORTION! 1
to 3 Sets of 5 to 15 seconds is plenty.

Assume the above position only the grey

leg is down (like the white). Tighten your
tummy and SLOWLY raise your knee
toward your chest. Keep that tummy tight
as you lower it back down to the ground.
Repeat with the other limb.
To make this more difficult, lift your head
off the ground as well and hold it up as

directions. 1 to 3 Sets of 5 to 20 repetitions with

each leg is enough.

For our final stomach exercise, lets combine the

above two exercises, only we will NOT go all the
way. Tighten the tummy and SLOWLY (like a Kung
Fu master) lift the left arm and right leg
SIMULTANEOUSLY. Bring them to the mid-way point
(12 O'clock), hold for 5 to 15 seconds, and return
them to their original positions. Repeat other side. 1
to 3 Sets of 5 to 20 repetitions with each leg is
enough.

you do the leg-ups. 1 to 3 Sets of 5 to 20

repetitions with each leg is enough. .
You can also use ankle weights if you are
tolerating these well.

Take two or even three pillows and lie on

top of them as shown above. Slowly raise
your left leg (keeping it straight) upward
and HOLD it at the top for 5 to 20
seconds. Slowly lower and repeat with the
other lower limb. Only raise your leg to a
comfortable height. DON'T go so high that
your causing a lot of pain. You don't have
to go very high for this to be effective. 1 to
3 Sets of 5 to 20 repetitions with each
leg is enough.

DO NOT DO THIS ONE IF YOU HAVE A BAD

NECK! Take two or even three pillows and lie on top
of them as shown above. Note that the pillows are
more forward (on the chest) than compared to the
'Prone Leg Extensions'. Also note that I use a little
pad for the forehead. Slowly raise your left arm
(keeping it straight) upward and HOLD it at the top
for 5 to 20 seconds. Slowly lower and repeat with
the other arm. Only raise your arm to a comfortable
height. You don't have to go very high for this to be
effective. 1 to 3 Sets of 5 to 20 repetitions with
each arm is enough.

DO NOT DO THIS ONE IF YOU HAVE A BAD

NECK! Take two or even three pillows and lie on top
of them as shown above. Simultaneously lift the
white arm (left) and grey leg (right) slowly upward.
Don't force it! just go as high as you can. Hold this
top position for 5 to 20 seconds and then lower.
Repeat the other limb pair. 1 to 3 sets of 5 to 20
repetitions with each limb pain (white arm - grey
leg) is good enough.

Here's an alternative to the exercise on

the left. Simply mount the Gym Ball as
shown above. Note that both knees touch
the ground. Next Slowly raise and extend
your right arm and HOLD it at the top for 5
to 20 seconds. Slowly lower and repeat
with the other arm. Only raise your arm to
a comfortable height. You don't have to go
very high for this to be effective. 1 to 3
Sets of 5 to 20 repetitions with each
arm is enough.

Start in the above position (grey). Make

sure your knees are spread fairly wide
apart so you have a good base. You can
put some pillows under your knees to
boost yourself up if need be. If you have
neck problems fold your arms across your
chest instead of the 'hands-behind-head
position. SLOWLY lift your chest off the
ball. DON'T TRY TO GET TO HIGH OFF
THE BALL at first. A little bit of 'lift' goes a
long way. HOLD that top position for 3 to
10 seconds and then slowly lower your
self back to the grey position. 1 to 3 sets
of 5 to 20 repetitions will be enough.

While keeping your low back in the neutral position,

simply sit for 5 to 20 minutes while watching TV.
You may bounce gently, and slightly roll from side to
side. Just 'play', but make sure you keep that neutral
spine.